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1
Zhao, Yuan. "Immunology of granulomatosis with polyangiitis". Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/immunology-of-granulomatosis-with-polyangiitis(91230752-735f-41ea-8695-f26f8b2e5c97).html.
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Granulomatosis with polyangiitis (GPA, formerly known as Wegener’s granulomatosis) is a rare and sometimes fatal systemic autoimmune disease. Anti-neutrophil cytoplasmic antibodies (ANCAs) specific for proteinase 3 (PR3) are associated with GPA. However, the pathogenesis of GPA is not yet clear. Our aim was to investigate the local autoimmune response, circulating immune modulatory cells and cells expressing the immune suppressor molecules programmed death 1 (PD-1) and its ligands in GPA. In mucosa from GPA patients, activated B cells were observed located alongside PR3 expressing cells and B cell survival factors BAFF and APRIL, which was produced by the granulomas and giant cells. B cells were proliferating and persistent in biopsies. However no evidence of B cell clones from the mucosal biopsies circulating in peripheral blood was observed in GPA. An increased frequency of circulating TFH cells and a reduced frequency of Treg cells was observed in peripheral blood from GPA patients on conventional therapies compared to healthy controls. No such difference was found in GPA patients treated with rituximab. The frequency of circulating TFH and Treg cells was found to be inversely correlated in human peripheral blood. No difference in the relative quantity of mRNA encoding PD-1 in lymphocytes and monocytes was found in GPA patients compared with healthy controls. Lower percentage of CD14+ monocytes expressing PD-1 was observed in GPA patients. Lower relative quantity of mRNA encoding PD-1 ligands PD-L1 and PD-L2 in T cells and monocytes was observed in GPA patients. In conclusion, data in this thesis identifies activated B cells alongside auto-antigens and B cell survival factors in the mucosa in GPA. A negative correlation between TFH and Treg cells is observed that implies the balance between T cell subsets and its B cell dependence are associated with disease activity in GPA. The deficiency of PD-L1 and PD-L2 mRNA in lymphocytes and monocytes may contribute to the pathogenesis of GPA.
2
Fashola, Bola. "The Effect of Sodium Chloride on Beta-Hemolytic Streptococci". TopSCHOLAR®, 1987. https://digitalcommons.wku.edu/theses/2321.
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The drug of choice for the treatment of Stieptococcal pharyngitis is penicillin G. However, a common home remedy prescribes the use of salt-water solutions for gargling.
Members of Beta -hemolytic streptococcal groups A, B, and C were isolated from the upper -respiratory tracts of patients diagnosed as having streptococcal pharyngitis. These cultures we:e obtained from HCA Greenview Hospital (Bowling Green, Kentucky) and used to study the effects of sodium chloride on the isolates.
The minimum inhibitory concentration of sodium chloride was determined for each of eight hospital isolates. Croup A streptococci were inhibited at a concentration of 7.2% sodium chloride while Group C streptococci were inhibited at a 7.0% concentration. Group P streptococci were more resistant, and inhibition of growth occurred at 12.0% sodium chloride concentrations.
Scanning electron microscopic studies showed no significant differences in the external structure of cells treated with sodium chloride when compared to non-treated cells. Despite the lack of changes in the external structure of treated cells, fine structural alterations were observed with transmission electron microscopic studies.
Treatment of the cells with sodium chloride resulted in a condensation of nucleoid deoxyribonucleic acid (DNA) and some loss of ribosomes. These changes were followed by a dissolution of the cytoplasmic cell contents resulting in an intact cell wall with capsule.
Other parameters such as the rate of growth, minimum bactericidal concentrations, DNA content and protein content of cells treated with sodium chloride were examined and compared to control cells.
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Ventevogel, Melissa Samo. "Cytokine Modulation of Thymopoiesis". NCSU, 2008. http://www.lib.ncsu.edu/theses/available/etd-03182008-100350/.
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The thymus is an organ derived from embryonic endoderm and mesoderm differentiation. It is located above the heart and is made up of two compartments, the thymic epithelial space and the perivascular space. The thymic epithelial space consists of the cortex and the medulla, which is where T cell development, maturation and induction of self tolerance occur in a process known as thymopoiesis. The thymus is susceptible to chronic and acute stressors that result in thymic involution. A consequence of thymic involution is reduced thymopoiesis, which affects the generation of a diverse T cell repertoire and establishment of central T cell tolerance. Many thymosuppressive and thymostimulatory cytokines are involved in thymopoiesis and thymic involution. Keratinocyte growth factor and IL-7 are two cytokines that function in driving early thymic progenitor proliferation and T cell development, respectively. We hypothesized that IL-7 and Keratinocyte growth factor, delivered via recombinant adenovirus, can improve thymopoiesis and T cell reconstitution in mice in an endotoxin model of acute thymic atrophy. Analysis of thymus weight, cellularity, phenotype and TCR gene rearrangement showed moderate increases in thymic function with delivery of IL-7 or Keratinocyte growth factor versus control. Taken together, these data suggested that IL-7 and Keratinocyte growth factor, delivered via recombinant adenoviruses, have thymostimulatory effects on the thymus in normal thymus or settings of acute thymic atrophy and maybe beneficial for future development as therapeutics.
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Chilcoat, Clayton Douglas. "Protein Kinase A Regulates β2 Integrin Avidity Activation and Subsequent Neutrophil Activation via Modulation of Myosin Light Chain Kinase". NCSU, 2005. http://www.lib.ncsu.edu/theses/available/etd-03312005-093042/.
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β2 integrins are adhesion molecules on the surface of neutrophils. Avidity activation of β2 integrins includes transportation of pre-formed integrins to the cell surface and a conformational change in the integrin to a high-binding state. Upon binding ligand, β2 integrins initiate a signaling cascade that results in activation of the neutrophil to a pro-inflammatory state, and the inhibition of this signal can prevent further activation of the neutrophil. cAMP and it effector protein kinase A (PKA) exert a generally inhibitory effect upon neutrophil activation. PKA has been shown to inactivate myosin light chain kinase (MLCK). Myosin light chain (MLC) phosphorylation is crucial for actin-myosin complex formation, which is required for stability and contraction of the actin cytoskeleton in neutrophils as well as β2 integrin-dependent adhesion. We hypothesize that the inhibitory effect of PKA upon neutrophils is due to inhibition of β2 integrin avidity activation resulting in the subsequent inhibition of neutrophil activation. Furthermore we hypothesize that the effect of PKA upon β2 integrin avidity activation is mediated through PKA?s effect upon MLCK. We demonstrate that inhibition of PKA induces β2 integrin-dependent adhesion and that augmentation of cAMP prevented β2 integrin-dependent adhesion and subsequent respiratory burst activity. Further, we demonstrate via flow cytometric detection of antibodies directed against β2 integrins that pharmacologic inhibition of PKA activity results in overall increased β2 integrin expression on the neutrophil surface, as well as increased expression of the activated form of the integrin. This upregulation and activation of β2 integrins due to inhibition of PKA is abolished by pharmacologic MLCK inhibition. Inhibition of MLCK also blocked β2 integrin-dependent neutrophil adhesion achieved by inhibition of PKA, as well as neutrophil migration along towards a PKA inhibitor. These findings demonstrate that PKA regulation of β2 integrin affinity activation and subsequent neutrophil activation is via an MLCK-dependent pathway.
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Pressler, Barrak. "The Role of Complementary Proteins in Autoimmune Glomerulonephritis". NCSU, 2008. http://www.lib.ncsu.edu/theses/available/etd-05062008-155750/.
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Although numerous theories exist proposing mechanisms whereby autoimmune diseases may be initiated, as of yet none of these have been definitively shown to be responsible for the induction of any naturally-occurring disease. One of these theories, known as autoantigen complementarity, states that the initiator of an autoimmune response may not be the target autoantigen itself or an exogenous mimic, but instead is a peptide or protein that is âantisenseâ or âcomplementaryâ in shape and/or charge to the autoantigen. The first immune response is therefore production of an antibody specific for this complementary protein, followed by an anti-antibody (i.e. anti-idiotypic antibody) that reacts with the paratope of the first antibody and also recognizes the âsenseâ or self-protein due to surface contour, charge, and/or hydropathy complementarity. Our laboratory group has published evidence for autoantigen complementarity in one autoimmune glomerular disease, proteinase-3 specific antineutrophil cytoplasmic autoantibody glomerulonephritis. The overall objective of the work described here was to provide further evidence for complementary proteins as inciting antigens in autoimmune glomerulonephritis using anti-GBM disease as the classic antibody-mediated autoimmune glomerulopathy; our central hypothesis was that anti-GBM disease is caused by a protein or peptide complementary to the anti-GBM autoantigen. The design of synthetic peptides complementary in sequence to portions of the human and rat α3(IV)NC1 collagen domains, and the design and production of a recombinant complementary α3(IV)NC1 protein more likely to possess appropriate tertiary structure to be complementary in sequence and in structure to the full-length anti-GBM epitope are described. These antigens were used to demonstrate that a subset of patients with anti-GBM disease have anti-idiotypic antibodies specific for α3(IV)NC1-complementary peptides and proteins, that these antibodies are distinct from their pathogenic idiotypic partners, and that the anti-GBM antibodies bind to these anti-complementary protein antibodies as expected by idiotypic:anti-idiotypic partners. Finally, we describe the immunologic and clinicopathologic consequences of immunization of two rodent models with anti-GBM-complementary peptides, thus providing provisional evidence for autoantigen complementarity-induced anti-GBM disease.
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Rogers, Melinda Cadd. "Differential thrombospondin expression on T lymphocytes in a Feline Immunodeficiency Virus model". NCSU, 2007. http://www.lib.ncsu.edu/theses/available/etd-06152007-103921/.
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CD4+CD25+ T regulatory cells represent an important subset of lymphocytes whose function is to suppress autoimmune disease and control normal immune responses. There is much research indicating a direct role for TGF-beta expressed on the surface of Tregs in the suppressor function of these cells. TGF-beta, whether bound to the cell surface or secreted, is produced as part of a complex that renders the cytokine inactive. Thrombospondin is the primary activator of biologically latent TGF-beta. This research demonstrates that thrombospondin is expressed on the surface of T lymphocytes isolated from the blood and lymph nodes of normal and FIV positive felines. Thrombospondin is expressed at significantly higher levels on CD4+CD25+ T lymphocytes, but can be induced in culture by activating T helper cells in the presence of LPS and IL2. We also observed that the CD4+CD25- T helper cells isolated from FIV negative control lymph nodes were able to markedly upregulate surface thrombospondin expression compared with similarly stimulated CD4+CD25- T helper cells from FIV positive sources. These findings are initial steps in working to understand the mechanism behind latent TGF-beta activation on CD4+CD25+ T regulatory cells and the role this cell type plays in FIV/HIV pathogenesis.
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lee, kang mi. "Antibody and Cellular Immune Responses of Swine Exposed to Porcine Reproductive and Respiratory Syndrome Virus or a GP5 Subunit Vaccine". NCSU, 2007. http://www.lib.ncsu.edu/theses/available/etd-07052007-104723/.
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Developing effective vaccines against the porcine reproductive and respiratory syndrome virus (PRRSV) has proved difficult, highlighting the need for basic information on the nature of the immune response against this virus and the mechanisms of resistance that the virus employs. In this investigation our goal was to characterize the immune response against the major outer membrane protein of the virus, GP5, in pigs experimentally infected with a North Carolina isolate of PRRSV known as the NC Powell strain. In addition, we compared this response with the immune response seen after vaccination with purified recombinant GP5 (rGP5) protein. Humoral immune responses were monitored by western blot and immunofluorescence while T cell responses were monitored using proliferation assays and flow cytometry. Our results show strong humoral recognition of rGP5 protein during both natural and vaccine induced Ab responses. In addition, epitope mapping via western blot revealed that Ab responses were directed largely against the C-terminal endodomain of rGP5 protein in both experimentally infected and vaccinated pigs. We also investigated T cell responses to rGP5 protein. Our experiments revealed that T cells from vaccinated animals also responded to both rGP5 protein and inactivated NC Powell strain of PRRSV suggesting that T cells may play an important role in vaccine-induced resistance. Interestingly, we found that the inactivated NC Powell strain of PRRSV caused a strong proliferative response in naïve T cells from control animals, perhaps indicating the presence of a superantigen as a component of this highly virulent strain of PRRSV.
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Madison, Sharon L. "THE EFFECTS OF PM2.5 ON ALLERGIC INFLAMMATION IN MAST CELL DEFICIENT MICE". NCSU, 2002. http://www.lib.ncsu.edu/theses/available/etd-05082002-132938/.
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MADISON, SHARON LYNN. The effects of PM2.5 on allergic inflammation in mast cell deficient mice. (Under the direction of Bruce Hammerberg.) Animal models of asthma have confirmed epidemiological findings that exposure to fine particulate matter (PM2.5) can enhance asthmatic symptoms, including eosinophilic inflammation and airway hyperresponsiveness. Critics have dismissed the possibility that these studies utilizing artificial exposure scenarios, like intratracheal instillation (i.t.), can be legitimately extrapolated to human risk largely due to the fact that the doses required for this type of model exceed the normal ambient concentrations of PM2.5. In order to improve the credibility of the findings from previous animal studies utilizing the i.t. method for delivery of aqueous particle suspensions to the lung, and to determine the biological mechanisms responsible for the observed enhancement of allergic inflammation following PM2.5 exposure, large-scale air samplers have been developed making it possible to directly expose wild type (WT) and genetically altered mice to fine, concentrated ambient particles (CAPs). In this study allergic asthma was modeled in both WT and mast cell deficient (MCD) mice by local (L) or systemic (S) sensitization to ovalbumin (OVA). Two weeks later mice were challenged with OVA (day 0) and then exposed to CAPs (day 0 & 1) with numerous endpoints collected (day 0-2). Overall, there was a temporal difference in the bronchoalveolar lavage cell profile between L and S sensitized mice, and the contribution of mast cells (MC) to this differential response was best observed for neutrophils at day 0 and day 1. Compared to air exposed mice, CAPs depressed total inflammatory cell infiltrates in the bronchoalveolar lavage fluid at day 0 and day 1 after OVA challenge for all groups. This overwhelming difference of limited cellular infiltration of monocytes and neutrophils in the bronchoalveolar lavage fluid following CAPs exposure, and the significant difference between the L and S sensitization protocols, confound interpretation for all of the factors examined. However, the specific finding that CAPs can enhance eosinophil recruitment by day 2 after OVA challenge indicates that the results from previous animal studies utilizing i.t. PM2.5 exposures do in fact support the epidemiological associations linking PM2.5 exposures with the enhancement of allergic inflammation indicative of the asthmatic phenotype. Given the strict regulation of immunological tolerance at mucosal surfaces like the lung, the genetic variability of different mouse strains, and the daily changes in ambient PM2.5 composition, the findings of this study prompt many unique questions. However, the bottom line is that this study demonstrates that ambient PM2.5 does alter Th2-like responses in mice by enhancing pulmonary BAL eosinophils in the late phase response (day 2), and that mast cells are critical to their recruitment.
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Chen, Hsin-Ying. "T CELL RESPONSE TO INFECTION BY THE PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS". NCSU, 2005. http://www.lib.ncsu.edu/theses/available/etd-01062005-170050/.
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The purpose of the research has been to characterize the response of naïve or virus-specific swine T lymphocytes from different lymphoid compartments to Porcine Reproductive and Respiratory Syndrome Virus (PRRSV). Peripheral blood mononuclear cells (PBMCs), tracheobronchial lymph node (TLN) and lateral retropharyngeal lymph node (LLN) cells were labeled with PKH67 green fluorescence dye to measure cell proliferation and surface phenotypes were examined using anti-CD4, anti-CD8 or anti-CD25 monoclonal antibodies. Stimulation with Concanavalin A was also included as a positive control. Our results show that potential virus-specific T lymphocytes were found in the peripheral blood, although no cell proliferation was found in cultures of lymph node cells. We did find that the percentages of CD8+ T cells in cultures of lymph node cells from the virus-infected pig increased after in vitro stimulation with the Powell virus compared to the lymph node cells cultured in media only, suggesting that CD8+ T lymphocytes may play a role in the virus clearance and immune memory to PRRSV.
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Emani, Sirisha. "MOLECULAR CHARACTERIZATION OF T REGULATORY CELLS IN FIV-INFECTION". NCSU, 2006. http://www.lib.ncsu.edu/theses/available/etd-01192006-105756/.
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Naturally occurring CD4+CD25+ T regulatory cells (Treg) play important roles in maintaining immunologic self-tolerance in addition to controlling the magnitude of anti-microbial immune responses. However, the capacity of these CD4+CD25+ Treg cells to control immune responses both in vivo and in vitro is not well established. CD4+CD25+ Treg cell-mediated suppression can control autoimmune diseases; transplantation tolerance and graft verses host disease and, in contrast hinder tumor immunity and immunity to infectious agents. As Treg cells have been reported to be involved in several diseases, this study focused on molecular characteristics that enables them to maintain anergy and also resistance to programmed cell death along with the effect of FIV-infection on regulation of the above phenotypic characteristics. Our results show that feline CD4+CD25+ Treg cells are phenotypically and functionally anergic as indicated by elevated levels of the cyclin dependent kinase inhibitors, CdkI¡¦s, (p21cip1,p16ink4, and p27kip1) , and resistance to mitogen-induced proliferation compared to their counter parts CD4+CD25- T cells. Importantly, CdkI¡¦s are constitutively over-expressed only in FIV-infected cats. As expected Treg cells from FIV-infected cats that over-expressed CdkI¡¦s expressed low levels of the cyclins (mainly cyclins D) and phosphorylated retinoblastoma protein (pRb) that are responsible for cell cycle progression. We investigated the role of TGF?Ò signaling and found that TGF?Ò1 plus ConA stimulation was able to convert CD4+CD25- T cells to CD4+CD25+ T cells with functional and phenotypic characteristics including upregulation of CdkI¡¦s and bcl-2. The differential expression of CdkI¡¦s and bcl-2 between the two CD4+ T cell subsets may be linked to TGF?Ò-Smad pathway. Consistent with upregulation of CdkI¡¦s and bcl-2, we found that although natural and TGF?Ò1 converted CD4+CD25+ Treg cells are anergic, they are more resistant to activation induced cell death compared to CD4+CD25- T cells functionally which correlated with increased bcl-2 to bax ratio in Treg cells. Thus, the molecular characterization of this unique population of Treg cells may be essential for understanding their role and function for developing effective therapeutics and vaccination especially against chronic infections such as Acquired Immune Deficiency Syndrome (AIDS).
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Eckert, Rachael. "Molecular Mechanisms of Neutrophil Migration". NCSU, 2007. http://www.lib.ncsu.edu/theses/available/etd-10312007-134315/.
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This work is an investigative look behind the mechanisms of neutrophil migration. Each of three chapters involves exploration into a different signaling pathway important for migration downstream of chemoattractant stimulation through inhibition of a kinase or disruption of the function of an effector and examination of the effects on migration, adhesion, and actin reorganization in primary human or equine neutrophils. Chapter II examines the requirement for the signaling molecule p38 Mitogen Activated Kinase (MAPK) in equine neutrophil chemotaxis through use of the p38 specific inhibitor SB203580. SB203580 reduced LTB4- and PAF-induced migration and disrupted the ability of cells to polarize, but did not affect b2 integrin-dependent adhesion or surface b2 integrin expression. Chapter III is a comprehensive inquiry into the regulation of the phosphorylation of serine 157 of the cytoskeletal protein Vasodilator-stimulated Phosphoprotein (VASP). The rapid and transient phosphorylation of VASP serine 157 corresponded with F-actin levels in chemoattractant-stimulated human neutrophils. fMLF-induced serine 157 phosphorylation was abolished by pretreatment with the PKA inhibitor H89 and the adenylyl cyclase inhibitor SQ22536. In contrast, fMLF-induced serine 157 phosphorylation was unaffected by PKC inhibitors, PKG inhibitors, and the CamKII inhibitor KN-62. Inhibition of adhesion did not alter fMLF-induced VASP phosphorylation or dephosphorylation. This study demonstrated that chemoattractant stimulation of human neutrophils induces a rapid and transient PKA-dependent and adhesion-independent VASP serine 157 phosphorylation. Chapter IV probed into the function of the actin binding protein and PKC substrate Myristoylated Alanine-Rich C-kinase Substrate (MARCKS) through utilization of a cell permeant peptide derived from the MARCKS myristoylated aminoterminus (MANS peptide). Treatment of isolated human neutrophils with 50 μM MANS, but not a scrambled control peptide, significantly inhibited their migration and adhesion in response to fMLF, IL8, or LTB4. MANS significantly reduced F-actin content in neutrophils 30s after fMLF-induced polymerization, but did not alter the ability of cells to polarize, spread, or upregulate surface b2 integrin expression. These data provided evidence that MARCKS, via its myristoylated aminoterminus, is a key regulator of neutrophil migration and adhesion.
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Liebrich, Walter. "Expert evaluation of an on-line course in clinical immunology". Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/96006.
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Thesis (MPhil)--Stellenbosch University, 2014.ENGLISH ABSTRACT: This assignment describes an evaluation by experts of an on-line course in Clinical Immunology offered to medical registrars and scientists as a supplement to a practical rotation. Because of a lack of agreement on what constitutes quality in e-learning and to avoid the customary focus on usability evaluation, an open-ended, interpretivist approach was used here which, while not entirely novel, was unusual in an e-learning environment. For this project it was decided to evaluate both content (subject matter) as well as instructional value using two groups of peers from various academic institutions, clinical immunology experts and e-learning experts. Feedback was obtained through participation in a focus group or in writing. Replies were much easier to obtain from the e-learning group. Five out of seven e-learning experts provided a response, versus three out of twenty subject matter experts. Eventually most of the feedback was obtained from colleagues from the home institution. Both groups made valuable, somewhat overlapping suggestions. Subject matter experts indicated that the course materials were of good quality and adequate on a postgraduate level. E-learning experts expressed concern about the ability of the course to facilitate learning and identified also some usability issues. Some of the findings may well apply to other settings. A number of five evaluators in each group appeared to give a good coverage within an open-ended approach. Expert peer review offered insights that neither student feedback nor self-reflection could. Rather than imposing evaluative criteria on the experts through the use of fixed checklists, the open-ended approach allowed them to cumulatively develop their own framework tailor-made for the course. The choice of subject matter plus e-learning experts may be helpful in similar situations of evaluating on-line courses where dual expertise is not readily available. The open-ended interpretivist approach can be used for formative evaluation only and may work well for courses that are still in development or where an amount of uncertainty about teaching effectiveness exists. Future efforts will likely focus on implementing the recommendations, identifying sustainable ways of quality review for the current course and similar open-ended evaluation of other courses.
AFRIKAANSE OPSOMMING: Die evaluering deur kundiges van ’n aanlyn-kursus in Kliniese Immunologie word in hierdie opdrag bespreek. Hierdie kursus word bykomend tot ‘n praktiese rotasie vir kliniese assistente (medies) en wetenskaplikes aangebied. Aangesien daar nie eenstemmigheid is oor wat gehalte in e-leer behels nie, en om die gebruiklike fokus op die evaluering van gebruiksmoontlikhede te vermy, is ’n interpreterende benadering in hierdie geval gebruik. Alhoewel hierdie benadering nie heeltemal nuut is nie, is die gebruik daarvan ongewoon in die eleer- omgewing. Daar is besluit om vakinhoud sowel as onderrigwaarde in hierdie projek te evalueer. Twee ewe-kniegroepe van verskillende akademiese inrigtings, kundiges in kliniese immunologie sowel as kundiges in e-leer is gebruik. Terugvoer is ontvang deur die deelname aan fokusgroeponderhoude of deur skriftelike terugvoer. Terugvoer is makliker van die e-leergroep verkry. Vyf uit die sewe e-leerkundiges het gerespondeer teenoor drie uit die twintig vakkundiges. Uiteindelik is die meeste terugvoer verkry van kollegas van die tuisinstelling. Beide groepe het waardevolle, maar dikwels oorvleuelende aanbevelings gemaak. Die vakkundiges het aangedui dat die kursusmateriaal van ’n goeie gehalte en geskik op ’n nagraadse vlak is. Die eleerkundiges het hul kommer uitgespreek oor die vermoë van die kursus om leer te fasiliteer en het ook ’n aantal kwessies ten opsigte van bruikbaarheid uitgewys. Sommige van die bevindinge kan moontlik ook in ander kontekste van toepassing wees. Dit het geblyk dat ongeveer vyf evalueerders in elke groep ’n goeie verslag met die oopvrae-benadering gegee het. Vakkundige ewe-kniebespreking het insigte opgelewer wat nie moontlik was met studente-terugvoer of selfrefleksie nie. In plaas daarvan dat evaluerende kriteria deur vaste vraelyste op die kundiges afgedwing is, het die oopvrae-benadering hulle die geleentheid gebied om kummulatief hul eie toepaslike raamwerk vir hierdie spesifieke kursus te ontwikkel. Die keuse van vakkundiges en e-leerkundiges mag nuttig wees in soortgelyke situasies waar aanlynkursusse geëvalueer word en die tweeledige kundigheid nie geredelik beskikbaar is nie. Die oopvraeinterpreterende benadering kan slegs vir formatiewe evaluering gebruik word en mag moontlik goed werk vir kursusse wat nog ontwikkel word en waar daar heelwat onsekerheid oor die doeltreffendheid van die onderrig bestaan. Verdere ontwikkeling sal waarskynlik fokus op die implementering van die aanbevelings, die identifisering van volhoubare maniere van gehalte-beoordeling vir die huidige kursus en soortgelyke oopvrae-evaluering van ander kursusse.
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Clauson, John. "Cryptococcus neoformans Serotype Groups Found in Clinical and Environmental Isolates". TopSCHOLAR®, 1993. http://digitalcommons.wku.edu/theses/1888.
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Cryptococcus neoformans is an encapsulated yeast responsible for severe meningoencephalitis. The importance of epidemiological studies on cryptococcosis has increased since the beginning of the AIDS epidemic. C. neoformans exists in two varieties containing four serotypes, C. neoformans var. neoformans (serotypes A and D) and C. neoformans var. gattii (serotypes B and C). Locally C. neoformans var. neoformans has been associated with pigeon feces during those months having an average temperature of 64.2°F j(17.8°C) and above. Clinical and environmental isolates of C. neoformans obtained from regional hospitals and environmental samplings, respectively, have been grouped into their variety status utilizing canavanine-glycine-bromthymol blue agar. Polyclonal antisera against C. neoformans serotypes A, B, C and D were isolated from challenged rabbits. Serotyping C. neofromans isolates using the polyclonal antisera resulted in 57% (20 of 35) of the serotypes confirmed with a direct immunofluorescent assay utilizing a single monoclonal antibody (E1). Data from the immunofluorescence assay suggest all C. neoformans obtained from regional hospitals (26 of 26) and those isolated from the environment (9 of 9) belong to the A serotype group. These data have provided information leading to the origin of infection for cryptococcosis in our region, which may be beneficial to immunocompromised individuals.
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Kell, Holly. "Effects of a Simulated Tennis Match on Lymphocyte Subset Measurements". TopSCHOLAR®, 2010. http://digitalcommons.wku.edu/theses/218.
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Research has shown that maximal exercise has a significant effect on cells of the immune system. Specifically, lymphocyte count increases during exercise and decreases to a value lower than baseline following an acute exhaustive bout of exercise. The overall lymphocyte response is well characterized, however, the ability of exercise to affect lymphocyte subfractions is unknown to our knowledge. The purpose of this study was to assess and evaluate the affects of a simulated tennis match across two sessions on lymphocyte subsets.
Initial measurements such as age, height, weight, skinfold analysis, and heart rate were recorded for each player, as well as blood samples being obtained by a finger prick before and after the tennis sessions. The tennis protocol started with five serves to the deuce court and five serves to the ad court, then individuals hit twenty-four forehands and twenty-four backhands against an oscillating ball machine. Each bout of serves and ground strokes were repeated ten times, with one minute rests in between each session. Before and immediately after completing the tennis trial, subjects were pricked with a lancet on the non dominant hand so to obtain at least two capillary tubes of blood. Whole blood was then added to the antibody cocktail, which is mixed according to the antibodies that were tested, which were CD4, CD8, CD19, CD95, and CX3CR1. Whole blood was added to red blood cell lysis buffer and fixation buffer, and the blood solution was incubated with antibodies specific to cell phenotype. The main results of this study indicated that there was a decrease in mainly post cell counts in pre and post CD19/CD95 measurements (P= .007), an increase in CD8/CX3CR1 in pre counts and an increase then decrease in post counts without wearing the bionic glove (P= .042), and a decrease in CD4 in the post count measurement with the bionic tennis glove (P= .043). The study’s can assist in making recommendations for after match treatment such as health and diet suggestions. Knowledge of prevention and treatment methods are low in the field of tennis and immune functions, so findings in this area could prevent elite athletes from contracting infections between matches.
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Garg, Himanshu. "Feline Immunodeficiency Virus (FIV) Envelope Glycoprotein-Mediated Cell Fusion and Apoptosis". NCSU, 2003. http://www.lib.ncsu.edu/theses/available/etd-11042003-141554/.
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Feline Immunodeficiency Virus (FIV) and Human Immunodeficiency Virus (HIV) are lentiviruses that are remarkable similar in their genomic organization, receptor usage and pathogenesis. Based on this FIV has evolved into a well-established small animal model for studying AIDS. FIV and HIV cause a progressive depletion of T cells via a still unknown mechanism though numerous studies support a role of membrane expressed HIV env glycoprotein in apoptotic killing of CD4+ T cells. HIV env glycoprotein is a heterodimer of surface expressed gp120 that binds to CD4 and a chemokine receptor and transmembrane gp41 that mediates fusion and syncytia formation. The role of the fusion process in HIV env-mediated apoptosis remains controversial even though evidence suggests that cytopathic effect of HIV is related to the fusogenic potential of env glycoprotein. Blocking HIV env receptor interactions either at the level of gp120 or gp41 blocks both syncytia formation and apoptosis. This suggests a crucial role for HIV gp41 in fusion, as well as apoptosis. The hydrophobic pre-transmembrane (pre-TM) region of HIV gp41 is important for membrane fusion and sequence analysis reveals a similar region in FIV gp41. The current study was undertaken to determine the role of different regions of FIV env in mediating fusion and apoptosis in bystander cells and to determine whether the two phenomena are related. FIV env interactions with target cells were blocked at the level of gp120 or gp41 and the effect of these on fusion and apoptosis studied. The role of FIV gp41 pre-TM region in fusion and apoptosis was also determined. Our findings support a role of FIV env in apoptotic loss of T cells and this phenomenon correlates with env-mediated fusion.
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Birkenheuer, Adam Joseph. "Canine Babesiosis: Epidemiological, Molecular and Therapeutic Investigations". NCSU, 2004. http://www.lib.ncsu.edu/theses/available/etd-04192004-164025/.
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Canine babesiosis is an emerging infectious disease in the United States (US). An epidemic of Babesia gibsoni infections in the US was identified. An association between dog breed and B. gibsoni infections was detected. Babesia gibsoni-infected dogs were more likely to be American pit bull terriers and B. canis vogeli infected dogs were more likely to be greyhounds. An association between a recent dog bite and B. gibsoni infection was detected, implicating direct dog-to-dog transmission as a route of infection in the US. Several genes from canine Babesia spp. were characterized, including 18S ribosomal RNA (rRNA), internal transcribed spacer regions (ITS), cytochrome B (cytB), and rhoptry-associated protein-1 (RAP-1). These genetic data were used to develop a sensitive and specific diagnostic semi-nested polymerase chain reaction (PCR) test for canine babesiosis. Using this assay, a novel large Babesia organism was identified in a blood sample obtained from a clinical patient. Molecular and phylogenetic characterization of this large Babesia spp. determined that it was most closely related to B. bigemina. Lastly, an atovaquone and azithromycin drug combination was shown to be the first treatment to clear canine B. gibsoni infections.
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Liu, Pinghuang. "Virus infection and evolution in the central nervous system following intracerebroventricular inoculation with Feline Immunodeficiency Virus". NCSU, 2005. http://www.lib.ncsu.edu/theses/available/etd-10302005-212859/.
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HIV-1 infection of the central nervous system (CNS) results in neurological impairments in subpopulation of HIV-infected individuals which range from from mild cognitive/motor disorder (MCMD) to HIV-associated dementia (HAD). HIV-1 associated neurological diseases are still a big problem even with the introduction of combined antiretroviral therapy. However the mechanisms of CNS infection and pathogenesis that lead to HAD are still not completely clear. HIV-1 CNS infection occurs soon after peripheral infection. Subsequent to infection, the CNS may act as a protected anatomical reservoir for lentiviruses and may also give rise to the development of or sequestration of unique quasispecies. The choroid plexus (ChP) has been demonstrated to be an important site for lentivirus infection and contains a mixture of viral quasispecies including both systemic and brain derived isolates. Since the appearance of viral RNA is particularly prominent in the cerebrospinal fluid (CSF), the ChP-CSF pathway may contribute to infection and viral diversity in the CNS. In the present study, we investigated lentiviral infection and evolution within the CNS by directly infusing virus into the CSF using an FIV animal model. Cell-free NCSU1 FIV or cell-associated FIV (FIV infected ChP macrophages) was directly injected into the right lateral ventricle of the brain. Negative controls were sham inoculated with uninfected ChP macrophages or cell-free culture supernatant and positive controls were infected systemically with cell-free FIV by intraperitoneal (i.p.) injection. Intracerebroventricular (i.c.v.) inoculation with cell-free FIV resulted in high levels of plasma FIV RNA detected as early as 1-2 weeks post inoculation in all 6 i.c.v. cats, and the plasma viremia preceded the detection of CSF viral RNA. Compared to i.p. cats, i.c.v. cats exhibited much higher levels of CSF FIV RNA and FIV DNA in the brain, increased ratios of CSF to plasma viral load (>1 at several time points), and a unique rebound CSF viral peak (5 of 6 cats). Infusion of FIV-infected ChP-Mac induced an acute inflammatory response and a slight suppression of the CD4+:CD8+ ratio, but failed to produce a detectable infection. After cell-free inoculation, FIV env variants, amplified by the poymerase chain reaction (PCR) and isolated using the heteroduplex tracking assay (HTA), exhibited clear compartmentalization between the CNS and periphery. Unique or enriched variants rapidly appeared in the CSF. Similar variation was seen in FIV proviral DNA isolated from cortical and subcortical brain regions. Compared to the initial viral peak in CSF, the second CSF viral peak displayed considerable change from both the first CSF peak and matched samples of plasma. FIV env diversity was highest in the CNS tissue and was unrelated to matched PBMCs collected at the same time indicating that the sequences were not due to PBMC trafficking. In addition, three unique variants were found to be selectively enriched in the CNS. Taken together, these results demonstrated that 1) CSF provides an efficient pathway for the transfer of infectious virus to the periphery, 2) virus trafficking through the CSF promotes infection of the CNS and viral diversification, 3) CSF virus may derive from both the local productive infection and blood, and 4)virus within the CNS experienced a relatively rapid and independent evolution relative to virus in the periphery.
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Mexas, Angela Marie. "CD4+CD25+ REGULATORY T CELLS ARE INFECTED AND ACTIVATED PHENOTYPICALLY AND FUNCTIONALLY DURING ACUTE INFECTION WITH FELINE IMMUNODEFICIENCY VIRUS". NCSU, 2007. http://www.lib.ncsu.edu/theses/available/etd-11022007-103144/.
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HIV-induced AIDS may be mediated by the activation of immunosuppressive CD4+CD25+ T regulatory cells (Tregs). Tregs have been shown to regulate CD4+ and CD8+ immune responses to HIV and FIV antigens in vitro. We tested the hypothesis that Tregs become infected and activated during the acute stage of FIV infection leading to the suppression of CD4+ T helper cell responses. Cats were experimentally infected with FIV-NCSU-1 and blood and lymph node biopsies were collected at 1 week intervals following inoculation. Real-Time PCR was used to determine plasma viremia and relative number of FIV copies in CD4+CD25+ and CD4+CD25- T cell subsets. Flow cytometry was used to assess the absolute numbers of each cell type and the expression of activation markers. Real-time RT-PCR was also used to assess relative increases in FoxP3 and TGF- mRNA levels over time. Treg suppression of IL-2 production in CD4+ T helper cells was assessed by ELISPOT assays and inhibition of cellular proliferation was assessed by incorporation of tritiated thymidine and CFSE. Our results show that peak viremia levels correlate with maximal infectivity in lymph node CD4+CD25+ populations. FIV-gag-mRNA levels are higher in CD4+CD25+ T cells than CD4+CD25- lymph node T cells. Activation of FoxP3 and increased expression of TGF1 in CD4+CD25+ cells correlates with peak plasma viremia and FIV-gag-mRNA levels in CD4+CD25+ T cells. Regulatory function can be detected in CD4+CD25+ T cells during the acute phase of FIV infection. Our findings support the hypothesis that early activation of immunosuppressor function in Treg cells may limit an effective anti-FIV response contributing to the establishment of the chronic infection and the immunodeficiency caused by this virus.
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Gowdy, Kymberly Mae. "Increased Susceptibility and Severity of Influenza in Mice Exposed to Diesel Exhaust". NCSU, 2008. http://www.lib.ncsu.edu/theses/available/etd-11202008-100143/.
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Epidemiological studies have noted an increase in adverse health effects with increasing levels of air pollution. One major area of concern is the incidence of respiratory infections, specifically influenza. An air pollutant that has raised concern in recent years is diesel exhaust (DE) due to an increase the amount of diesel engines in use. Previous laboratory studies have reported that DE exposure prior to an influenza infection increases viral titers but the mechanism of how this occurs is still unknown. Herein, studies were designed to investigate three main areas associated with DE enhanced influenza infection. 1) Assess whether DE affects host defense responses against pathogens, 2) Determine if pre-exposure to DE increases susceptibility to influenza in vivo, 3) Investigate whether exposure to DE increases the severity of an ongoing established influenza infection. DE exposure alone increased proinflammatory cytokines, adhesion molecules, decreased expression and production of surfactant proteins (SP)-A and D as well as clara cell secretory protein (CCSP). The molecules downregulated by DE are important for binding viral and bacterial pathogens therefore making the lung more susceptible to infection. This was confirmed when mice were exposed to DE and then subsequently infected with influenza A. One day post infection mice pre-exposed to DE had a significant increases in influenza induced inflammation and viral titers that were associated with a decrease in SP-A and SP-D. Mice exposed to DE during an established influenza infection also had a significant increase in viral titers and pulmonary inflammation throughout the course of infection. This DE-enhanced influenza infection was associated with an upregulation of the Th2 cytokine IL-4 which has previously been shown to delay clearance. However with antioxidant treatment to combat the oxidative stress induced by DE, pulmonary inflammation and IL-4 expression returned to baseline levels. Taken together these data indicate that exposure to DE either before or during influenza infection has immunomodulatory effects that can be detrimental to the host with increased viral proliferation and morbidity associated with the disease.
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Wiczynski, Teresa. "Interactions between Aerobic Exercise Volume, Academic Stress, and Immune Function". TopSCHOLAR®, 2018. https://digitalcommons.wku.edu/theses/2334.
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Many college students exercise individually or participate in collegiate and intramural sports in addition to fulfilling their stressful academic requirements. The combination of accumulated stress and vigorous exercise could result in an impaired immune system, prompting the onset of disease and absences in class and sports practice.
Twenty-six male and female participants aged 18 to 23 were recruited for this study. Over the course of an academic semester, participants completed weekly electronic surveys documenting stress levels, aerobic exercise, and symptoms related to upper respiratory tract infections. Participants were evaluated at four different time points (Baseline, Post-Midterm Exam, Baseline Reassessment, and Post-Final Exam) for body fat percentage, cardiovascular fitness, heart rate, blood pressure, and a 10mL blood draw. Blood samples were used to measure blood glucose, cortisol, IL-6, and CD11b levels. Analysis of cortisol and IL-6 concentrations required ELISA kits for protein quantification in plasma samples. CD11b levels in peripheral blood mononuclear cell samples were measured by Western Blot analysis.
There was a significant increase in blood pressure during the final exam compared to rest for systolic (p=0.005) and diastolic (p=0.004) blood pressures. There was a significant decrease in anxiety during the final exam compared to anxiety during the mid-term exam (p=0.022). The acute stress of an exam was strong enough to illicit physiologic blood pressure change, but the chronic stress throughout the semester was not intense enough did not illicit physiologic or immune responses. The volume of aerobic exercise in the vigorous workout group was not great enough to influence immune responses nor disease incidence.
21
Harkin, Damien Gerard. "Morphological responses of neutrophils in suspension to plasma components and chemotactic factors /". Title page, contents and summary only, 1992. http://web4.library.adelaide.edu.au/theses/09PH/09phh282.pdf.
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Gnanasampanthan, Gnanapragasam. "Immune responses of sheep to rumen ciliates and the survival and activity of antibodies in the rumen fluid". Title page, contents and abstract only, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phg571.pdf.
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Videorecording has title: Effect of antibodies on the motility of rumen ciliates. Bibliography: leaves 197-259. Consists of a review of rumen ciliates, their implications in ruminant nutrition and a description of the research methods, the results and the conclusions drawn with regard to the prospects of establishing an immunological basis for the manipulation of rumen ciliates.
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Clayer, Mark. "The phagocytic function of regenerated splenic tissue /". Title page, contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09MD/09mdc6222.pdf.
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Faull, Randall James. "Studies of vascular endothelial cell surface antigens relevant to the alloimmune response". Title page, table of contents and abstract only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09phf2634.pdf.
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Bibliography: leaves 234-314. Examines the role of vascular endothelial cells in inflammation with particular reference to their participation in the immune response directed against a vascularised allograft (kidney)
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Wong, Yu Hin. "Highly pathogenic avian influenza (H5N1) in Hong Kong, 1997-2014 : towards an urban biopolitical immunology". Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/highly-pathogenic-avian-influenza-h5n1-in-hong-kong-1997--2014-towards-an-urban-biopolitical-immunology(dde69f59-8dd0-48ee-819f-c5ef98d3b0b1).html.
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The thesis traces the successive urban responses made by the Hong Kong government from 1997 to 2014, in an attempt to achieve “imagined immunity” for the city. The urban responses being analysed are efforts to regulate the ways in which “live poultry” (especially live chickens) is metabolized and circulating in the city. The efforts are made to re-order the human-birds-microbes relationships in Hong Kong - a process conceptualized as “re-urbanization of nature.” The consequence of these re-urbanization of nature processes, led to changes in the specific practice of consuming “live poultry” in the city. Four periods of re-urbanization of nature are identified in the analysis, and it is argued that in each wave of restructuring there were markedly different frames constructed to generate distinctive meanings of the “contagion condition,” imagined urban immunity, and practices of re-urbanization of nature. Their meanings and resultant practices were products of negotiations, within an entangled web of human and nonhuman features in particular periods. The context of these interventions and the biopolitical contestations are analyzed in the thesis. It is then argued that such contingencies and context-sensitive processes, call for further studies of post-epidemic urban changes. The thesis also explores the possibility of developing a theoretical framework of “urban biopolitical immunology” to accomplish the inquiry. By so doing, it seeks to contribute to studies of the politics of contemporary epidemics, and to research on the production of urban nature.
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Thompson, Fiona Marie. "Activation of the mucosal immune system and growth of the small intestine at weaning /". Title page, abstract and contents only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09pht4677.pdf.
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Stroher, Vive Horst. "Serotype conversion in Vibrio cholerae 01 /". Title page, contents and abstract only, 1992. http://web4.library.adelaide.edu.au/theses/09PH/09phs919.pdf.
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Moghaddami, Mahin. "Characterization of isolated lymphoid aggregations in the mucosa of the small intestine /". Title page, abstract and contents only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phm6959.pdf.
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Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1999.Errata & addenda tipped in behind back end paper. Copies of author's previously published articles in pocket on back end-paper. Bibliography: leaves 147-194.
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Smailhodzic, Armin. "Adapting the Standard SIR Disease Model in Order to Track and Predict the Spreading of the EBOLA Virus Using Twitter Data". TopSCHOLAR®, 2015. http://digitalcommons.wku.edu/theses/1465.
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A method has been developed to track infectious diseases by using data mining of active Twitter accounts and its efficacy was demonstrated during the West African Ebola outbreak of 2014. Using a meme based n-gram semantic usage model to search the Twitter database for indications of illness, flight and death from the spread of Ebola in Africa, principally from Guinea, Sierra Leone and Liberia. Memes of interest relate disease to location and severity and are coupled to the density of Tweets and re-Tweets. The meme spreads through the community of social users in a fashion similar to nonlinear wave propagation- like a shock wave, visualized as a spike in Tweet activity. The spreading was modeled as a system isomorphic to a modified SIR (Susceptible, Infected, Removed disease model) system of three coupled nonlinear differential equations using Twitter variables. The nonlinear terms in this model lead to feedback mechanisms that result in unusual behavior that does not always reduce the spread of the disease. The resulting geographic Tweet densities are coupled to geographic maps of the region. These maps have specific threat levels that are ported to a mobile application (app) and can be used by travelers to assess the relative safety of the region they will be in.
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Hudson, Sarah. "Myeloid antigen presenting cell populations in the murine uterus /". Title page, abstract and contents only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phh887.pdf.
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Varikuti, Sanjay. "Role of CD4+CD25+ Regulatory T Lymphocytes in Experimental Toxoplasmosis". TopSCHOLAR®, 2009. http://digitalcommons.wku.edu/theses/113.
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Toxoplasmosis is an important cause of congenital disease, and it is one of the most common opportunistic infections in patients with acquired immunodeficiency syndrome. The need for a reliable experimental model of this infection is crucial not only for achieving a better understanding of the patho-physiology of the disease, but also for developing better methods for evaluating new therapeutic regimens. The purpose of the present study was to investigate the role of CD4+CD25+ T regulatory lymphocytes in mice infected with Toxoplasma gondii. T regulatory (Treg) cells have been shown to play an important role in our immune system in controlling the activity of other T lymphocytes. These cells are differentiated from other T lymphocyte populations based on the co-expression of CD4 and CD25 and expression of the Foxp3 gene. The results of several recent studies have suggested that certain pathogens may be able to increase their survival in the host by exploiting T reg cell activity. T regulatory cells have been shown to control the persistence of the protozoan parasite, Leishmania major, in mice; however, this population of cells plays only a limited role during murine infection with Trypanosoma cruzi. In the present study we have investigated the role of Treg cells during murine infection with the ME49 strain of T. gondii. In vivo depletion of Treg cells was accomplished by injecting mice with a monoclonal antibody (Mab) isolated from the 7D4 rat hybridoma cell line. This Mab is specific for the interleukin-2 receptor chain (also known as CD25). Female Swiss Webster mice of approximately 6-7 weeks of age were depleted of Treg cells by intraperitoneal injection of 400µg of Mab, mice were injected once 7days prior to infection, and a second time 1 day prior to infection, with 20 tissue cysts of T. gondii. Mouse weight and tissue cyst numbers were monitored to evaluate the impact of Treg depletion on the outcome of infection. Our results suggest that depletion of Treg cells has little measurable impact during the acute stage of infection with the ME49 strain of T. gondii. Further studies will be required to determine what role, if any, these cells play in the chronic stage of murine toxoplasmosis.
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Reel, Michael Stephen. "The Role of Ectopic Lymphoid Tissue in Allograft Rejection". Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06282006-140255/.
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The location of the immunologic response to an allograft is not known with certainty. However, organized collections of T cells, B cells and antigen presenting cells have been found in peripheral tissue, in close proximity to organs undergoing rejection. It is hypothesized that this tertiary lymphoid tissue may be a location in which activation of lymphocytes can occur, leading to rejection of an allograft. We report here that in a splenectomized aly/aly mouse, which is devoid of secondary lymphoid organs and will normally fail to reject an allograft, the presence of tertiary lymphoid organs is associated with graft rejection. We additionally find that tertiary lymphoid organs can act as lymph nodes, and can support effector and memory allograft rejection responses. It is demonstrated that ectopic lymphoid tissue in aly/aly mice will support the multiplication and transformation of transferred naïve CD4 and CD8 T cells into cells that display phenotypic markers characteristic of effector and memory lymphocytes. These results demonstrate that ectopic lymphoid tissue is associated with the loss of immunologic ignorance and is sufficient to enable graft rejection. This suggests that allograft rejection may take place within ectopic lymphoid tissue, and suggests that techniques to interfere with the development of this tissue might offer a therapeutic approach to preserving organ allografts.
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Li, Dongmei. "Immune reactions involved in parasitoid-host interactions /". Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phl6926.pdf.
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Clark, Anel. "Development and validation of an in vitro model of dendritic cell identification and activation". Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/21605.
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Thesis (MScMed)--Stellenbosch University, 2008.ENGLISH ABSTRACT: The aim of this study was to investigate the effect of MBV and Coley’s Toxin on dendritic cells in vitro. The dendritic cell system of antigen presenting cells is the initiator and modulator of the immune response. The principle function of the dendritic cells is to present antigens to resting naïve T lymphocytes: these cells are the only APCs that prime naïve T cells and only mature DCs can carry out this function.Previous studies done on dendritic cells showed that bacterial peptides can induce the maturation of dendritic cells. With the results of these studies in mind we hypothesized that these two vaccines will also induce the maturation of dendritic cells. Chapter 1 is a literature review on the immune system explaining the organs and cells of the immune system. Chapter 2 includes a full description of DCs, the MBV and Coley’s toxin. Also included in this chapter is a short explanation of the principle of the technique being used for the identification and maturation of both mDCs and pDCs, namely the technique of flow cytometry. Chapter 3 describes the method for the phenotypic identification of DCs: the subsets are distinguished by their absence of expression of several lineage markers for lymphocytes, monocytes and NK cells and the expression of CD11c (in the case of myeloid DCs) and CD123 (in the case of plasmacytoid DCs). The inclusion of HLA-DR in addition to the previous described markers allows the discrimination of CD123+ DCs from basophils. The assay requires three tubes per sample which enables quick analysis of these rare subsets with a small sample volume. This assay was applied to peripheral blood samples obtained from healthy individuals and individuals with cancer, HIV and HIV and TB co-infected patients. Our results showed that the maturation status of DCs in HIV and lymphoma were low but those measured in the case of HIV + TB patients were even higher than in the control group. Chapter 4 and 5 describe the in vitro activation and maturation status of DCs following their incubation with bacterial-derived products. Interactions between DCs and microbial pathogens are fundamental to the generation of innate and adaptive immune responses and upon contact with bacteria or bacterial components such as lipopolysaccharide (LPS), immature DCs undergo a maturation process that involves expression of costimulatory molecules, HLA molecules, and cytokines and chemokines, thus providing critical signals for lymphocyte development and differentiation. In this study, we investigated the response of human DCs to MBV and Coley’s Toxin. Previous studies showed DCs can be activated with killed Streptococcus pyogenes. With this study in mind it was hypothesized that the MBV and Coley’s Toxin used in this study might modulate DC maturation. The results of this study showed that the MBV and Coley’s toxin did induce the maturation of both pDCs and mDCs as measured by increased surface expression of costimulatory molecules such as CD80 and CD83. Chapter 6 presents the measurement of cytokines released after the PMBCs had been were incubated with Coley’s Toxin and Mixed Killed bacteria. The BD™ Cytometric Bead Array (CBA) flex set was used for the simultaneous detection of multiple soluble analytes. The results indicated that both Coley’s Toxin and the MBV activated the DCs and subsequently induced TH1 as well as a TH2 responses in the T cells present in the cell cultures. Finally, a general conclusion discussing the significance and implications of our results as well as possible future research required is discussed in Chapter 7. DCs are potent antigen presenting cells (APCs) which play a critical role in the regulation of the immune response. There is great interest in exploiting DCs to develop immunotherapies for cancer, chronic infections, immunodeficiency diseases and autoimmune diseases.
AFRIKAANSE OPSOMMING: Die doel van die studie was om die effek van ‘n gemengde bakteriële vaksiene en Coley se toksiene op dendritiese selle te toets in vitro. Die dendritiese sel sisteem speel ‘n belangrike rol in die modulering en reaksie van die immuun sisteem.Die hoof funksie van dendritiese selle is om antigene bloot te stel aan naïewe ongeaktiveerde T selle. Slegs volwasse dendritiese selle kan die T selle aktiveer. Vorige studies het bewys dat bakteriële peptiedes die veroudering van die dendritiese selle kan induseer. Met die resultate in gedagte het ons gehipotiseer dat die twee vaksienes ook die maturasie van dendritiese selle kan induseer. Hoofstuk 1 is ‘n literatuur studie wat handel oor die organe en selle van die immuun sisteem. Hoofstuk 2 gee n volle beskrywing van dendritiese selle, die gemengde bakteriële vaksiene en Coley se toksiene. Ingesluit in die hoofstuk is die beskrywing van die prinsiep van die tegniek, vloei sitometrie, wat gebruik word vir die identifikasie en veroudering status van die dendritiese selle. Hoofstuk 3 beskryf ‘n vloei sitometrie metode vir die fenotipiese identifikasie van dendritiese selle. Dendritiese sel tipes kan onderskei word deur die afwesigheid van sekere merkers vir limfosiete, monosiete en NK selle. Plasmasitoïede dendritiese selle druk CD123 uit en miloïede dendritiese selle druk CD11c uit. HLA DR is ook ingesluit saam met die bogenoemde merkers om die dendritiese selle te onderskei van basofiele. Vir elke toets word slegs drie buise geprosesseer en dus kan die subklasse vinning geanaliseer word. ʼn Klein volume bloed word benodig vir die toests. Perifêre bloed is gebruik vir die toets op bloed monsters van 10 gesonde individue en individue met kanker, HIV en HIV en TB. Die resultate van die studie het getoon dat die maturasie status van die dendritiese selle in HIV en limfoom was, maar in die geval van HIV en TB pasïente was die maturasie status selfs hoër as die van die kontrole groep. Hoofstuk 4+5 beskryf die aktivering en maturasie status van die dendritiese selle na inkubasie met die bakteriële produkte. Interaksie tussen dendritiese selle en patogene speel ‘n belangrike rol in die aktivering van die immuunstelsel. Wanneer dendritiese selle in aanraking kom met bakterieë of bakteriële komponente, matureer die dendritiese sel wat lei tot the uitdrukking van stimulerings molekules, HLA molekules end die uitskeiding van sitokiene. Die uitdrukking van die molekules lei tot limfosiet ontwikkeling en differensiasie. In die studie het ons gekyk na die reaksie van menslike dendritiese selle in die teenwoordigheid van die gemende bakteriële vaksiene en Coley se toksiene. Vorige studies het bewys dendritiese selle word geaktiveer deur Streptococcus pyogenes. Met die resultate in gedagte het ons gehipotetiseer dat die gemengde bakteriële vaksiene en Coley se toksiene ook die maturasie van dendritiese selle kan induseer. Die resultate van die studie het bewys dat die gemengde bakteriële vaksiene en Coley se toksiene die veroudering van beide pDCs en mDCs induseer. Die uitdrukking van verouderings merkers CD80 en CD83 is gemeet. Hoofstuk 6 beskryf ‘n vloei sitometrie metode om die sitokiene te meet wat afgeskei word nadat selle geinkubeer het in die teenwoordigheid van Coley se toksiene en die gemengde bakteriële vaksiene.Die BDTM CBA Flex set metode het dit moontlik gemaak om meer as een sitokiene te meet in net een buis Die resultate het getoon dat albei die vaksienes ‘n TH1 en TH2 reaksie veroorsaak. Laastens volg‘n algemene afleiding waar ons kyk na die toepassing en implikasies van die resultate asook toekomstige navorsings moontlikhede,word bespreek in Hoofstuk 7 Dendritiese selle speel ‘n kritiese rol in die regulering van die immuun reaksie. Verdere studies kan nou gedoen word om dendritiese selle terapeuties toe te pas vir die behandeling van kanker, autoimmuniteit, immuun onderdrukkende siektes en kroniese siektes.
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Parsa, Roham. "Macrophage activation phenotypes in type 1 diabetes pathogenesis and therapy : Master thesis". Thesis, KTH, School of Biotechnology (BIO), 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-10210.
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Macrophages are an important key effector cell in the immune system which can practically be found in every tissue. Macrophages have for a long time been considered a population of cells only responsible for pro-inflammatory responses and anti-microbial activities. But over the past decade, many have come to realize the amazing plasticity of macrophages in response to different stimulations. The anti-microbial and pro-inflammatory macrophage is known as classically activated macrophages but newly discovered phenotypes have been revealed named wound-healing macrophages and regulatory macrophages. Through systematic screening we have identified an inducible macrophage activation state which has both wound-healing and regulatory capabilities activated by the novel cytokine combination IL-4/IL-10 with or without TGF-β.
36
Botes, Annelise. "Immunological and epidemiological investigations in South African ostriches and penguins". Thesis, Stellenbosch : Stellenbosch University, 2004. http://hdl.handle.net/10019.1/53747.
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Dissertation (PhD)--University of Stellenbosch, 2004ENGLISH ABSTRACT: Newcastle disease (NO) and mycoplasma infections in ostriches have considerable economic implications for the South African ostrich industry in that NO is a limiting factor in the export of ostrich products to the European Union and mycoplasma infections cause stock losses, reduced production, reduced hatchability and downgrading of carcasses. In the first section of this dissertation, the role of passively acquired and mucosal immunity in protection of ostrich chicks against Newcastle disease virus (NOV) was investigated. Ostrich hen serum IgG and yolk IgY were isolated and characterized, and the transfer of maternal anti-NOV antibodies to the egg yolk was determined using an enzyme-linked immunosorbent assay (ELISA). Results indicated that anti-NOV antibodies were successfully transferred from the ostrich hen to the egg yolk. In addition, ostrich IgA was isolated, characterized and rabbit anti-ostrich IgA antibodies produced and used for measuring mucosal anti- NOV IgA antibodies produced in response to mucosal vaccination. Results indicated that the live La Sota vaccine stimulates IgA production and thus mucosal immunity in ostrich chicks. In the second section of this dissertation, ostrich mycoplasmas were isolated and identified using 16S rRNA gene sequencing. These sequences indicated that ostriches carry three unique mycoplasmas, which are phylogenetically quite divergent. The 16S rRNA gene sequences of the ostrich mycoplasmas were subsequently used for the development of specific primers for the detection and diagnosis of mycoplasma infections in ostriches by PCR. The last section of this dissertation focuses on avian malaria in African penguins and the management of this disease during rehabilitation. The Foundation for the Conservation of Coastal Birds (SANCCOB) is a seabird rescue and rehabilitation centre, which is largely dedicated to the rehabilitation of diseased, injured and oiled penguins. Significant mortalities due to avian malaria occur at this facility. The aim of this study was the development of an ELISA for the purpose of assessing the natural levels of anti-Plasmodium antibodies in African penguins on entry into the SANCCOB facility and during rehabilitation. Results indicated significant increases in anti- Plasmodium antibody levels after entry, which was not influenced by oiling. Infection with malaria and not parasite recrudescence was viewed to be the cause of this increase, indicating a possible role of the SANCCOB facility in exposing penguins to avian malaria.
AFRIKAANSE OPSOMMING: Newcastlesiekte (NS) en mikoplasmainfeksies in voltruise het geweldige ekonomiese implikasies vir die Suid-Afrikaanse volstruisbedryf. Die rede hiervoor is dat NS 'n beperkende faktor in die uitvoer van volstruisprodukte na die Europese Unie is, en mikoplasmainfeksies tot kudde verliese, verlaagde produksie en uitbroei asook lae gradering van karkasse lei. In die eerste gedeelte van hierdie proefskrif is die rol van passiewe- en mukosale-immuniteit in die beskerming van volstruiskuikens teen NS virus (NSV) ondersoek. Volstruishenserum IgG en eier IgY is geïsoleer en gekarakteriseer en die oordrag van maternale anti-NSV antiliggame na die eier ondersoek met behulp van 'n 'enzyme-linked immunosorbent assay' (ELISA). Resultate het getoon dat anti-NSV antiliggame suksesvol van die hen na die eier oorgedra is. Volstruis IgA is ook geïsoleer, gekarateriseer en konyn anti-volstruis IgA antiliggame geproduseer wat gebruik is vir die bepaling van mukosale anti-NSV IgA antiliggame in reaksie op mukosale immunisering. Resultate het getoon dat lewendige La Sota entstof IgA produksie stimuleer en dus tot mukosale-immuniteit in volstruiskuikens lei. In die tweede gedeelte van hierdie proefskrif is volstruismikoplasmas geïsoleer en geïdentifiseer met behulp van 16S rRNA geenopeenvolgingsbepalings. Hierdie volgordes het getoon dat drie unieke mikoplasmas in volstruise voorkom wat filogeneties verskillend blyk te wees. Die 16S rRNA geenopeenvolgings van die volstruismikoplasmas is gebruik vir die ontwikkeling van spesifieke inleiers vir die PKR identifisering en diagnose van mikoplasmainfeksies in volstruise. Die laaste gedeelte van hierdie proefskrif fokus op voëlmalaria in die Afrika pikkewyn en die bestuur van hierdie siekte gedurende rehabilitasie. Die 'South African Foundation for the Conservation of Coastal Birds' (SANCCOB) is 'n seevoëlreddingsen rehabilitasie-sentrum vir siek, beseerde en ge-oliede pikkewyne. Hierdie sentrum het egter aansienlike vrektes as gevolg van voëlmalaria. In hierdie studie is 'n ELISA ontwikkel vir die bepaling van natuurlike anti-Plasmodium antiliggaamvlakke van pikkewyne by aankoms en tydens rehabilitasie by SANCCOB. Resultate het 'n toename in anti-Plasmodium antiliggaamvlakke getoon na toelating wat nie beïnvloed is deur olie nie. Hierdie toename kan toegeskryf word aan nuwe malariainfeksies en nie 'n heruitbraak van bestaande infeksies nie wat daarop dui dat pikkewyne aan voëlmalaria blootgestel word by die SANCCOB-sentrum.
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Van, der Merwe Elizabeth Frances. "Preliminary investigations into ostrich mycoplasmas : identification of vaccine candidate genes and immunity elicited by poultry mycoplasma vaccines". Thesis, Stellenbosch : Stellenbosch University, 2006. http://hdl.handle.net/10019.1/17411.
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Thesis (MSc)--University of Stellenbosch, 2006.ENGLISH ABSTRACT: Ostrich farming is of significant economical importance in South Africa. Three ostrich mycoplasmas, Ms01, Ms02 and Ms03 have been identified previously, and were provisionally named ‘Mycoplasma struthiolus’ (Ms) after their host Struthio camelus. Ostrich mycoplasmas are the major causative organisms of respiratory diseases, and they cause stock losses, reduced production and hatchability, and downgrading of carcasses and therefore lead to large economic losses to the industry. In order to be pathogenic to their host, they need to attach through an attachment organelle, the so-called tip structure. This structure has been identified in the poultry mycoplasma, M. gallisepticum, and is made up of the adhesin GapA and adhesin-related CrmA. Currently, no ostrich mycoplasma vaccine is commercially available and for this reason the need to develop one has arisen. Therefore the first part of this study was dedicated to the identification and isolation of vaccine candidate genes in the three ostrich mycoplasmas. Four primer approaches for polymerase chain reactions (PCR’s), cloning and sequencing, were used for the identification of adhesin or adhesin-related genes from Ms01, Ms02 and Ms03. The primer approaches revealed that the target genes could not be identified due to the high diversity of sequences that were generated. Therefore sequences were also compared with those of other mycoplasma species in BLAST searches. Results showed that the most significant hit was with the human pathogen M. hominis oppD, which is located in the same operon as the membrane protein P100 involved in adhesion. Other hits were with ABC transporters which may also play a role in cytadhesion. The second part of this study was aimed at testing whether two poultry mycoplasma vaccines, M. synoviae and M. gallisepticum, can be used in ostriches to elicit immune responses until an ostrich mycoplasma vaccine has been developed. Ostriches on three farms of different age groups in the Oudsthoorn district were therefore vaccinated with these vaccines in a vaccine trial. The enzymelinked immunosorbent assay (ELISA) was used to test the level of antibody response. Results showed that both vaccines elicited an immune response in all three age groups. A high percentage of the ostriches reacted positively, which indicates that both vaccines elicit antibody responses and may therefore give protection against ostrich mycoplasma infections.
AFRIKAANSE OPSOMMING: Volstruisboerdery is ‘n belangrike ekonomiese sektor in Suid-Afrika. Drie volstruismikoplasmas, Ms01, Ms02 en Ms03, is voorheen geïdentifiseer en voorlopig ‘Mycoplasma struthiolus’ (Ms) benaam na aanleiding van hul gasheer, Struthio camelus. Volstruismikoplasmas is die grootste oorsaaklike organismes van respiratoriese siektes, kudde verliese en die afgradering van karkasse wat lei tot groot ekonomiese verliese in die volstruisbedryf. Ten einde patogenies vir die gasheer te wees, moet mikoplasmas deur middel van ‘n aanhegtingsmeganisme vasheg – die sogenaamde puntvormige struktuur. Hierdie struktuur is in die pluimvee mikoplasma M. gallisepticum geïdentifiseer, en bestaan uit aanhegting proteïen GapA en die aanhegting verwante proteïen CrmA. Tans is geen volstruismikoplasma entstof kommersieel beskikbaar nie, en derhalwe het die behoefte ontstaan om so ‘n entstof te ontwikkel. Die eerste gedeelte van hierdie studie is dus gewy aan die identifisering en isolering van entstof kandidaat gene in al drie volstruismikoplasmas. Vier inleier benaderings vir polimerase ketting reaksies (PKR), klonering asook geenopeenvolging bepalings vir die identifisering van aanhegting of aanhegting verwante gene vanuit Ms01, Ms02 en Ms03 is gebruik. Die inleier benaderings het getoon dat die teikengene nie geïdentifiseer kon word nie as gevolg van hoë variasie in die gegenereerde geenopeenvolgings. Derhalwe is geenopeenvolgings met ander mikoplasma spesies deur middel van BLAST soektogte vergelyk. Resultate het getoon dat die betekenisvolste ooreenstemming dié met die menslike patogeen M. hominis oppD was, wat deel vorm van die membraan proteïen P100 operon wat betrokke is by aanhegting. Ander ooreenstemmings sluit ABC transporters in wat moontlik betrokke kan wees by aanhegting. Die tweede gedeelte van hierdie studie het ten doel gehad om te toets of twee pluimvee mikoplasma entstowwe, M. synoviae en M. gallisepticum, gebruik kan word in volstruise om immuunresponse te ontlok tot tyd en wyl ‘n volstruismikoplasma entstof ontwikkel is. Volstruise vanaf drie plase in verskillende ouderdomsgroepe in die Oudtshoorn distrik was ingeënt met hierdie entstowwe in ‘n entstof proefneming. Die ensiem-afhanklike immuno-absorpsie essaï (ELISA) was gebruik om antiliggaam response te toets. Die resultate het getoon dat beide entstowwe immuunresponse ontlok het in al drie ouderdomsgroepe. ‘n Groot persentasie van die volstruise het positief gereageer wat ‘n aanduiding is dat beide entstowwe immuunresponse ontlok het en kan dus beskerming bied teen volstruismikoplasma infeksies.
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Zhang, Min Fen. "The role of milk transforming growth factor-[beta](TGF-[beta]) in the development of the infant gut and gut mucosal immune system". Title page, contents and abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phz51.pdf.
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In title, [beta] is represented by the Greek letter. Copies of author's previously published articles inserted. Errata pages pasted onto back end-paper. Bibliography: leaves 104-137. Studies milk TGF-[beta] and its receptors in the post-natal gut using a rat model to investigate a link between milk TGF-[beta] and the development of the infant gut and gut mucosal immune system. Finds maternal milk may be a major source of TGF-[beta] to the immature gut and may react with receptors on the cells of the mucosal immune system along the gastro-intestinal tract, modulating infant mucosal immune responses in the transition to the post-natal enteral feeding.
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Sritunyalucksana, Kallaya. "Characterisation of Some Immune Genes in the Black Tiger Shrimp, Penaeus monodon". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5087-3/.
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Brand, Anneke Mari. "Therapeutic properties of the lantibiotic nisin F". Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/79873.
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Thesis (PhD)-- Stellenbosch University, 2013.ENGLISH ABSTRACT: Bacterial resistance against antibiotic treatments is a global concern and resistance to almost every known antibiotic has already been reported. There is thus a significant need for the development of novel antimicrobial drugs. In addition to probiotic traits, certain bacteria have the ability to produce antimicrobial peptides, referred to as bacteriocins. Lantibiotics, a group of small ribosomally synthesized bacteriocins, recently gained interest for their application in the medical field. Lantibiotics have a very specific structure, including lanthionine rings, that stabilise the peptides. Due to their small size and specific action, these peptides reach specific sites of infection without affecting the composition of the host’s natural microbiota. As with any therapeutic agent, antimicrobial peptides are also prone to in vivo degradation, binding, clearance via immune action and development of bacterial resistance. Nisin F, a class Ia lantibiotic produced by Lactococcus lactis subsp. lactis F10, has already shown activity against the well-known pathogens Stapylococcus aureus, Listeria monocytogenes and various antibiotic resistant strains. The aim of this study was to assess the antimicrobial activity of nisin F against systemic S. aureus infections in mice and possible immune responses elicited by the peptide. A single administration of nisin F to the peritoneal cavity protected mice from S. aureus infection for at least 15 min. After continuous administration, the peptide showed no significant antimicrobial activity against S. aureus. The peptide did, however, convey some degree of protection to infected mice by stimulating a pro-inflammatory action through lymphocyte protection. When administered to uninfected mice, nisin F had an immune boosting effect via interleukin (IL)-6 and IL-10 without being detrimental to the host. The ex vivo effects of nisin F was compared to nisin A, a natural nisin variant, and Nisaplin®, a commercially purified form of nisin A. None of the three peptides inhibited the functional capacity of leukocytes in terms of 1L-1β en IL-6 production, not even in the presence of an external stimulus (lipopolysaccharides from Escherichia coli). Cytotoxicity was detected in response to high dosages of nisin F. Serum inhibited the antimicrobial effect of nisin F and nisin A, but Nisaplin® remained unaffected. Nisin F was applied against systemic infection for the first time and the immunological effect of the peptide was investigated. Nisin F partially protected mice against S. aureus infections through immunomodulatory effects. This study provided valuable knowledge on the in vivo application of nisin F. With further optimization of nisin F preparation and application systems, the peptide might be more effective against in vivo infections.
AFRIKAANSE OPSOMMING: Bakteriële weerstand teen antibiotika wek wêreldwyd kommer en weerstand teen amper elke bekende antibiotikum is reeds aangemeld. Daar is dus 'n groot behoefte vir die ontwikkeling van nuwe antimikrobiese middels. Bykomend tot probiotiese eienskappe, het sekere bakterieë die vermoë om antimikrobiese peptiede, bekend as bakteriosiene, te produseer. ‘n Groep klein ribosomaal-gesintetiseerde bakteriosiene, lantibitiotika, is onlangs vir mediese toepassing oorweeg. Lantibiotika beskik oor 'n baie spesifieke struktuur, insluitend lantionien ringstrukture, wat die peptied stabiliseer. Weens hul klein grootte en spesifieke aksie is hierdie peptiede daartoe in staat om spesifieke areas van infeksie te bereik sonder om die gasheer se natuurlike mikrobepopulasie te beïnvloed. Soos met enige terapeutiese middel, is bakteriosiene ook geneig tot in vivo afbreking, binding, klaring via die immuunsisteem en ontwikkeling van bakteriële weerstand. Nisien F, 'n klas Ia lantibiotikum, deur Lactococcus lactis subsp. lactis F10 geproduseer, het reeds aktiwiteit teen die bekende patogene Stapylococcus aureus, Listeria monocytogenes en verskeie antibiotika-weerstandige stamme getoon. Die doel van hierdie studie was om die antimikrobiese aktiwiteit van nisien F teen sistemiese S. aureus infeksies in muise te bepaal, asook die moontlike immuunreaksies wat die peptied mag veroorsaak. 'n Enkele toediening van nisien F het muise vir ten minste 15 min teen S. aureus beskerm. Na deurlopende administrasie het die peptied geen beduidende antimikrobiese aktiwiteit teen S. aureus getoon nie. Die peptied het egter 'n mate van beskerming aan geinfekteerde muise verleen deur ‘n pro-inflammatoriese aksie te inisieer deur limfosiet beskerming. Met toediening aan gesonde diere, het nisien F 'n immuunversterkende effek teweeg gebring via interleukin (IL)-6 en IL-10 vlakke, sonder nadelige uitwerking op die gasheer. Die ex vivo effek van nisien F is ook vergelyk met nisien A, 'n natuurlike variant van nisien, asook Nisaplin®, 'n kommersieël-gesuiwerde vorm van nisien A. Nie een van die drie peptide het leukosiete se funksionele kapasiteit in terme van 1L-1β en IL-6 produksie inhibeer nie, selfs nie in die teenwoordigheid van ‘n eksterne stimulus (lipopolisakkariede van Escherichia coli) nie. Seltoksisiteit is na blootstelling aan hoë dosisse van nisien F waargeneem. Serum het die antimikrobiese effek van beide nisien F en nisien A geïnhibeer, terwyl die werking van Nisaplin® nie beïnvloed is nie. Nisien F is vir die eerste keer teen sistemiese infeksies ingespan en die immunologiese impak van die peptied is ondersoek. Nisien F het gedeeltelike beskerming aan muise met S. aureus infeksies verleen deur die immuunsisteem te versterk. Die resultate het ‘n waardevolle bydrae gelewer tot die in vivo toediening van nisien F. Met verdere optimisering van nisien F voorbereiding en toedieningsisteme, mag die peptied moontlik meer effektief teen in vivo infeksies aangewend word.
The National Research Foundation (NRF) of South Africa for financial support and funding of the research
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Masjedi, Mohsen. "Physiological inflammation of the small intestine during weaning in the rat /". Title page, table of contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phm3973.pdf.
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Dobrescu, Gelu. "Mannose and Lipopolysaccharide Receptors on the Surface of Granular Hemocytes from the Crayfish Procambarus clarkii". [Johnson City, Tenn. : East Tennessee State University], 2002. http://etd-submit.etsu.edu/etd/theses/available/etd-0307102-133116/unrestricted/dobrescug032602.pdf.
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Goins, Kimberly R. "Host Defense Mechanisms in the Crayfish: the Effect of Injection with Live or Killed Bacteria". [Johnson City, Tenn. : East Tennessee State University], 2003. http://etd-submit.etsu.edu/etd/theses/available/etd-0328103-141532/unrestricted/Goins04162003f.pdf.
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Thesis (M.S.)--East Tennessee State University, 2003.Title from electronic submission form. ETSU ETD database URN: etd-0328103-141532. Includes bibliographical references. Also available via Internet at the UMI web site.
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Atkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha /". Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha878.pdf.
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Bonato, Maud. "Mate choice and immunocompetence in ostriches (Struthio camelus)". Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/1257.
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Thesis (PhD (Botany and Zoology))—University of Stellenbosch, 2009.Females of many bird species prefer to mate with males exhibiting elaborate ornamentation, which serves as an indicator of male quality. Such ornaments, called secondary sexual traits, could act as signals to females that males could confer direct and/or indirect genetic benefits (when offspring inherit superior genes), on offspring. In particular, it has been suggested that these signals relate to male ability to resist infections, as only high quality individuals are able to invest both in high immune defence and elaborate ornament expression. The ostrich (Struthio camelus) is the largest living bird and is a member of the family of flightless birds, the ratites. They are sexually dimorphic, males displaying black plumage, and a pink-coloured neck and bill; whereas females display dull-brown plumage (both sexes have white feathers). Little is known about the mating system of ostriches: they are promiscuous and in the wild, males and females have multiple partners. The communal nesting system of ostriches is unique in that only the major female and major male provide parental care, in the form of incubation and guarding the offspring until independence. Furthermore, a remarkable feature of cohorts is that offspring may differ greatly in size, and these size differences are likely to have a genetic basis arising from differing parental genotypic differences. As a trade-off between immune response and life-history traits has been documented in various bird species, I examined the relationships between male secondary sexual traits (and specifically colouration) and maternal investment; levels of immunocompetence in both parents and chicks; and chick growth. This study showed that females invest more at the egg stage in response to traits involved in the male courtship display: the colour of the neck, white and black body feathers, and the brightness of black feathers. As these traits, which are exposed during the courtship display as well as during male-male interactions, were related to male immune responses, I suggest that only high quality males will be able to display their condition optimally. Chicks with higher growth rates were found to have intermediate responses to stimulation of their humoral immune system with diphtheria and tetanus vaccines, suggesting that not only fitness benefits, but also costs are associated with mounting an immune response; and that variation in humoral responses and growth rates relates to how individuals trade off these costs and benefits. In addition, chick humoral responses were found to be related to the humoral response of both parents, but through different antibody responses (maternal responses to tetanus and paternal responses to diphtheria), suggesting that this component of the immune system is heritable. As the colouration of white feathers predicted chick growth rates, as well as a male’s ability to raise an antibody response, I suggest that this visual cue could serve as a signal to females of male humoral immunocompetence, therefore forming the basis of mate choice whereby females could increase the fitness of their offspring through higher growth rates.
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Thiart, Hanlie. "Immunological and epidemiological investigations into avian malaria in the African penguin during rehabilitation and in breeding colonies". Thesis, Stellenbosch : University of Stellenbosch, 2005. http://hdl.handle.net/10019.1/16620.
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Thesis (MSc)--University of Stellenbosch, 2005.ENGLISH ABSTRACT: The African penguin, which occurs along the south-eastern and south-western shores of South-Africa and Namibia, has experienced a severe reduction in population numbers due to guano and egg collection in the first half of the 19th century, and oil pollution in the second half of the 19th century as a result of oil tankers rounding the Cape of Good Hope. The population would have been reduced by a further 19% had it not been for the rehabilitation of penguins at the South African National Council for the Conservation of Coastal Birds (SANCCOB) facility. Although this has been very successful, mortalities as a result of avian malaria infection have considerably reduced the efficiency of rehabilitation. In an effort to assess the role of immunity against malaria in combating the disease, an enzyme-linked immunosorbent assay (ELISA) for the detection of antibody levels to avian malaria was developed. The ELISA was used to detect antibody levels to avian malaria of penguins on entry and during rehabilitation from October 2001 to January 2003. The aim of this study was to continue the determination of antibody levels to avian malaria of penguins entering the SANCCOB facility, in order to allow an evaluation of the antibody levels to avian malaria for two full calendar years. This investigation was combined with a polymerase chain reaction (PCR)-based method, capable of detecting any Plasmodium species in penguin serum. These two methods were also used to investigate avian malaria in several breeding colonies in order to assess the role avian malaria may play in the survival of the African penguin in the wild. Results indicated that the ability of penguins to produce anti-Plasmodium antibodies was not influenced by oiling and that infection with malaria was not due to recrudescence but rather due to infection via mosquitoes. This indicated a possible role of the SANCCOB facility in exposing the penguins to avian malaria. However a large number of penguins arrived at the facility previously infected with malaria, indicating that malaria was present in the breeding colonies. Investigations in the breeding colonies revealed extremely high avian malaria prevalence even though no sick birds or mortalities were observed. This raised the question whether different types of malaria are responsible for infection in the SANCCOB facility and breeding colonies.
AFRIKAANSE OPSOMMING: Die Afrika Pikkewyn kom langs die suid-oostelike en suid-westelike kus van Suid Afrika en Namibië voor. In die afgelope eeu het hierdie spesie ‘n geweldige afname in populasie getalle ondervind. Dit was hoofsaaklik die gevolg van die versameling van guano en pikkewyneiers in die eerste helfte van die 19de eeu en oliebesoedeling in die tweede helfde van die 19de eeu. Die “South African Foundation for Conservation of Coastal Birds” (SANCCOB) is ‘n seevoëlreddings- en rehabilitasiesentrum vir siek, beseerde en ge-oliede pikkewyne. Dit word geskat dat die Afrika Pikkewyn populasie met ‘n verdere 19% sou afgeneem het as dit nie vir die rehabilitasie by die SANCCOB sentrum was nie. Hierdie sentrum het egter aansienlike vrektes in die somer as gevolg van voëlmalaria, wat sodoende die effektiwiteit van die rehabilitasie verlaag. In ‘n poging om die rol van immuniteit teen malaria te bepaal is ‘n “enzyme-linked immunosorbent assay” (ELISA) ontwikkel vir die bepaling van antiliggaam vlakke teen malaria. Hierdie ELISA is gebruik vir die bepaling van die anti-Plasmodium antiliggaam vlakke van die pikkewyne by aankoms en ten tye van rehabilitasie by SANCCOB vanaf Oktober 2001 to Januarie 2003. Die doel van hierdie studie was eerstens om hierdie ELISA bepalings voort te sit om sodoende antiliggaam vlakke teen malaria oor twee kalender jare te kan evalueer. Hierdie ondersoek was gekombineer met ‘n polimerase ketting reaksie (PCR) metode, wat enige Plasmodium spesie in pikkewynserum sou kon opspoor. Hierdie twee metodes is ook gebruik vir ondersoeke in sommige broeikolonies, met die doel om te bepaal watter rol voëlmalaria in die oorlewing van die Afrika pikkewyn in die natuur speel. Resultate het getoon dat olie nie die vermoë van die pikkewyn beïnvloed om anti- Plasmodium antiliggame te vervaardig nie en dat malaria infeksie hoofsaaklik deur muskiete veroosaak word en nie deur heruitbraak van ‘n bestaande infeksie nie. Dit dui egter daarop dat pikkewyne blootgestel word aan voëlmalaria by die SANCCOB sentrum. Daar is ook gevind dat ‘n groot aantal pikkewyne met malaria infeksies by die sentrum opgedaag het wat dui op die voorkoms van malaria in die broeikolonies. Ondersoeke in die broeikolonies het ‘n besonder hoë voorkoms van malaria onthul. Geen vrektes of siek pikkewyne is in die broeikolonies waargeneem nie, wat moontlik kan beteken dat pikkewyne by SANCCOB met ‘n ander tipe malaria geïnfekteer word as in die broeikolonies.
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Lemmey, Andrew Bruce. "Effects of insulin-like growth factors (IGFS) on recovery from gut resection in rats : a thesis submitted to the University of Adelaide, South Australia for the degree of Doctor of Philosophy". 1992, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phl554.pdf.
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Includes bibliographical references (leaves 159-213) Shows that IGF-I peptides are effective in diminishing post-surgical catabolism and enhancing adaptive gut hyperplasia in rats recovering from massive small bowel resection.
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Zancanaro, Krauss Maria Eduarda. "CD4+ T cell metabolism during Trichuris muris infection". Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/cd4-t-cell-metabolism-during-trichuris-muris-infection(24eb0cc7-db70-46ea-ba49-e4fe3d5a5d03).html.
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Trichuris trichiura is a gastrointestinal dwelling nematode that infects almost 500 million people worldwide. T. muris occurs naturally in mice and is very closely related the human whipworm, making it a suitable model to dissect the immune response against the parasite. Studies using the Trichuris muris system have identified CD4+ T cells as dictators of the outcome of infection. In wild type mice, infection with a high dose of T. muris eggs leads to resistance and worm expulsion, which are dependent on a Th2 response and the secretion of type 2 cytokines especially interleukin (IL) 13. Chronicity is dependent on a Th1 response and occurs when mice are infected with a low dose of T. muris eggs. It is well established that metabolic changes are essential to promoting T cell activation and effector function. Moreover, during chronic infection the host immune system is continuously exposed to parasite antigen, which represents a metabolic challenge. This thesis has investigated the importance of T cell metabolism during response against T. muris. Data presented here show that low and high dose T. muris infections promote upregulation of the glycolytic pathway in CD4+ T cells. During later stages of chronic infection, CD4+ T cells displayed supressed glycolysis and mitochondrial respiration, and may be due to metabolic modulation imposed by the parasite. Leucine uptake via the amino acid transporter Slc7a5 was previously shown to be required for mTORC1 activation and for T cell effector function. Data presented here show that in early stages following a high dose T. muris infection, mice that lack Slc7a5 in T cells have delayed worm expulsion, impaired production of antibodies, and lower levels of IL-13. Their CD4+ T cells present reduced glycolytic rates when compared to cells from cohoused infected wild type mice. However, at later stages of infection, antibody, IL-13 and glycolytic levels were restored together with worm expulsion. CD4+ T cells from the early stage of infection showed reduced phosphorylation of mTOR, which suggested that impairment of function was mTOR dependent. Indeed, mice lacking mTOR in T cells fail to expel a high dose of parasites. They showed abrogation of IL-13 production, impairment in antibody class switching and their CD4+ T cells failed to upregulate glycolysis. Thus, this thesis shows that mTOR is essential for the proper functioning of T cells during T. muris infection and efficient amino acid transport plays a significant role. Taken together, these data show that metabolic orchestration of T cell function influences the capacity to effectively control helminth infection and that even subtle changes in T cell metabolic control can have a major effect on response phenotype.
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Purins, Leanne Roslyn. "Molecular characterisation of the transcriptional activator, HLYU, of Vibrio cholerae O1 /". Title page, abstract and table of contents only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09php9857.pdf.
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Thesis (Ph.D.)--University of Adelaide, School of Molecular and Biomedical Science , Discipline of Microbiology and Immunology, 2005."May, 2004" Includes corrigenda. includes bibliographical references (leaves 118-156).
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Mulhearn, Ben. "Identifying immune biomarkers to predict treatment response to biologic drugs in rheumatoid arthritis". Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/identifying-immune-biomarkers-to-predict-treatment-response-to-biologic-drugs-in-rheumatoid-arthritis(c311fc8c-4239-444a-9912-ddd4fde5f7fa).html.
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Rheumatoid arthritis (RA) is a chronic, heterogeneous, autoimmune disease that causes inflammation of synovial joints leading to pain, stiffness and swelling. If left untreated, RA results in irreversible joint destruction and long term disability. Initial treatment with glucocorticoids and other immunosuppressive agents suppresses inflammation. However, many of these drugs are not well-tolerated due to extensive side effects or are simply ineffective. The discovery of tumour necrosis factor-α (TNF) as a key mediator of inflammation in RA led to the development of monoclonal anti-TNF antibody therapy. Since then, other biologic drugs targeting immune pathways have been developed for RA, including interleukin-6 (IL-6) blockade, B cell depletion, and T cell co-stimulation blockade. Not all patients will respond to their first biologic drug and currently there is no way to predict which patient will respond to each different class of drug. Generally, 3 – 6 months are required to determine clinical efficacy, during which time joint inflammation proceeds. Therefore, discovering biomarkers to predict treatment response is a research priority. Biologic drugs target immune pathways. As single cell technology advances and has increasing capacity to identify subtle changes in many cell subsets, I hypothesise that studying the blood immune cell landscape will define cellular biomarker profiles relevant to each individual patient’s disease.