Letteratura scientifica selezionata sul tema "Streptococcus pneumoniae – immunologie"
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Articoli di riviste sul tema "Streptococcus pneumoniae – immunologie"
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Palmer, D. L. "Laboratory Diagnosis of Streptococcus pneumoniae Pneumonia". Journal of Infectious Diseases 151, n. 2 (1 febbraio 1985): 378. http://dx.doi.org/10.1093/infdis/151.2.378.
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Abateneh, Dejene Derseh, Abera Kumalo Shano e Teshale Worku Dedo. "Nasopharyngeal Carriage of Streptococcus pneumoniae and Associated Factors among Children in Southwest Ethiopia". Open Microbiology Journal 14, n. 1 (30 luglio 2020): 171–78. http://dx.doi.org/10.2174/1874285802014010171.
Testo completoAbstract (sommario):
Background: In Ethiopia, Streptococcus pneumoniae is the predominant causative agent of pneumonia. About, 95% of bacterial pneumonia cases in under five years of children are caused by pneumococci. Objective: To assess the nasopharyngeal carriage of Streptococcus pneumoniae, its antibiotic susceptibility pattern, and associated factors among children in Southwest Ethiopia. Methods: A cross-sectional study was conducted from October 01, 2018, to December 30, 2018. A total of 293 children aged ≤15 years were included in the study using a systematic random sampling technique. A nasopharyngeal swab was collected using a sterile cotton swab and cultured on blood agar supplemented with 5μg/ml gentamicin. The antimicrobial susceptibility testing was performed using the Kirby-Bauer disc diffusion technique. Results: The ages of participants ranged from 5 months to 14 years. The carriage rate of Streptococcus pneumoniae was 74/293 (25.3%). Being within the age group <3 years, the habit of sleeping with parent(s)/guardians and numbers of rooms per household were significantly associated with pneumococcal carriage. Streptococcus pneumoniae showed the highest resistance to Tetracycline, 36 (48.65%), and Trimethoprim/sulfamethoxazole, 29 (39.2%), and was found to be susceptible to Chloramphenicol, 54 (77%), and Erythromycin, 38 (51.4%). Conclusion: The nasopharyngeal carriage rate of Streptococcus pneumoniae is considerably high. High antimicrobial resistance of Streptococcus pneumoniae against Tetracycline and Trimethoprim/sulfamethoxazole was observed. Living in a house with a single room, children’s habit of sleeping with parents/guardians and age are associated factors of high pneumococcal carriage. Strategies need to be designed to address the modifiable associated factors and the bacterium antibiotic resistance pattern should be monitored regularly.
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Ahn, Danielle, e Alice Prince. "Participation of Necroptosis in the Host Response to Acute Bacterial Pneumonia". Journal of Innate Immunity 9, n. 3 (2017): 262–70. http://dx.doi.org/10.1159/000455100.
Testo completoAbstract (sommario):
Common pulmonary pathogens, such as Streptococcus pneumoniae and Staphylococcus aureus, as well as the host-adapted pathogens responsible for health care-associated pneumonias, such as the carbapenem-resistant Klebsiella pneumoniae and Serratia marcecsens, are able to activate cell death through the RIPK1/RIPK3/MLKL cascade that causes necroptosis. Necroptosis can influence the pathogenesis of pneumonia through several mechanisms. Activation of this pathway can result in the loss of specific types of immune cells, especially macrophages, and, in so doing, contribute to host pathology through the loss of their critical immunoregulatory functions. However, in other settings of infection, necroptosis promotes pathogen removal and the eradication of infected cells to control excessive proinflammatory signaling. Bacterial production of pore-forming toxins provides a common mechanism to activate necroptosis by diverse bacterial species, with variable consequences depending upon the specific pathogen. Included in this brief review are data demonstrating the ability of the carbapenem-resistant ST258 K. pneumoniae to activate necroptosis in the setting of pneumonia, which is counterbalanced by their suppression of CYLD expression. Exactly how necroptosis and other mechanisms of cell death are coregulated in the response to specific pulmonary pathogens remains a topic of active investigation, and it may provide potential therapeutic targets in the future.
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Briones, Maria Luisa, José Blanquer, David Ferrando, Maria Luisa Blasco, Concepción Gimeno e Julio Marín. "Assessment of Analysis of Urinary Pneumococcal Antigen by Immunochromatography for Etiologic Diagnosis of Community-Acquired Pneumonia in Adults". Clinical and Vaccine Immunology 13, n. 10 (ottobre 2006): 1092–97. http://dx.doi.org/10.1128/cvi.00090-06.
Testo completoAbstract (sommario):
ABSTRACT The limitations of conventional microbiologic methods (CMM) for etiologic diagnosis of community pneumococcal pneumonia have made faster diagnostic techniques necessary. Our aim was to evaluate the usefulness of the immunochromatography (ICT) technique for detecting urinary Streptococcus pneumoniae antigen in the etiologic diagnosis of community-acquired pneumonias (CAP). This was a prospective study on in-patients with CAP in a tertiary hospital conducted from October 2000 to March 2004. Apart from using CMM to reach an etiologic diagnosis, we determined pneumococcal antigen in concentrated urine by ICT. We also determined the urinary pneumococcal antigen (UPA) content in patients from two control groups to calculate the specificity of the technique. One group was comprised of in-patients diagnosed with chronic obstructive pulmonary disease (COPD) or asthma, with respiratory infection, and without pneumonia; the other group included fractures. We studied 959 pneumonia patients and determined UPA content in 911 (95%) of them. We diagnosed the etiology of 253 cases (28%) using CMM; S. pneumoniae was the most common etiologic agent (57 cases). ICT analysis was positive for 279 patients (31%). Using this technique, the percentage of diagnoses of pneumococcal pneumonias increased by 26%, while the overall etiologic diagnosis increased from 28 to 49%. The technique sensitivity was 81%; the specificity oscillated between 80% in CAP with nonpneumococcal etiology and 99% for patients with fractures without infections. Determination of UPA is a rapid, simple analysis with good sensitivity and specificity, which increased the percentage of etiologic diagnoses. Positive UPA may persist in COPD patients with probable pneumococcal colonization or recent pneumococcal infections.
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Mizgerd, J. P., B. B. Meek, G. J. Kutkoski, D. C. Bullard, A. L. Beaudet e C. M. Doerschuk. "Selectins and neutrophil traffic: margination and Streptococcus pneumoniae-induced emigration in murine lungs." Journal of Experimental Medicine 184, n. 2 (1 agosto 1996): 639–45. http://dx.doi.org/10.1084/jem.184.2.639.
Testo completoAbstract (sommario):
The roles of selectins in the pulmonary margination and emigration of neutrophils were investigated by using mice genetically deficient in both E- and P-selectins (E/P mutants) and/or by intravenous injections of fucoidin (inhibiting both L- and P-selectins). E/P mutants were neutrophilic (14.7 +/- 4.9 x 10(6) vs. 0.8 +/- 0.1 x 10(6) neutrophils/ml). This neutrophilia was associated with increased margination of neutrophils within pulmonary capillaries (39.7 +/- 9.4 vs. 4.6 +/- 1.1 neutrophil profiles per 100 red blood cell profiles) but no change in margination within noncapillary pulmonary microvessels. After intratracheal instillation of Streptococcus pneumoniae, lungs of E/P mutants displayed increased neutrophil emigration (564 +/- 92 vs. 116 +/- 19 neutrophils per 100 alveolar profiles), edema (5.3 +/- 1.5 vs. 1.5 +/- 0.4 microliter/g body weight), and histologic evidence of lung injury compared with those in wild-type (WT). Fucoidin treatment did not affect neutrophil emigration during streptococcal pneumonia in WT or E/P mice. During pneumonia, the number of white blood cells (WBC) tethered to or spread upon the noncapillary vessel endothelium increased in both WT and E/P lungs. These are the first data demonstrating that neutrophil margination in uninfected pulmonary capillaries does not require E- and P-selectins; that streptococcal pneumonia induces an E- and P-selectin-independent increase in WBC interactions with noncapillary endothelium; and that migration of neutrophils to alveoli can occur despite deficiency or inhibition of all of the known selectins.
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Peng, Xin, Yi Wu, Xiao Kong, Yunxiu Chen, Yonglu Tian, Qinyuan Li, Xiaoyin Tian, Guangli Zhang, Luo Ren e Zhengxiu Luo. "Neonatal Streptococcus pneumoniae Pneumonia Induces an Aberrant Airway Smooth Muscle Phenotype and AHR in Mice Model". BioMed Research International 2019 (6 gennaio 2019): 1–8. http://dx.doi.org/10.1155/2019/1948519.
Testo completoAbstract (sommario):
Our previous study showed that neonatal S. pneumoniae infection aggravated airway inflammation and airway hyperresponsiveness (AHR) in an OVA-induced allergic asthma model. As airway smooth muscle (ASM) plays a pivotal role in AHR development, we aim to investigate the effects of neonatal S. pneumoniae pneumonia on ASM structure and AHR development. Non-lethal neonatal pneumonia was established by intranasally infecting 1-week-old BALB/C mice with the S. pneumoniae strain D39. Five weeks after infection, the lungs were collected to assess the levels of α-SMA and the contractile proteins of ASM. Our results indicate that neonatal S. pneumoniae pneumonia significantly increased adulthood lung α-SMA and SMMHC proteins production and aggravated airway inflammatory cells infiltration and cytokines release. In addition, the neonatal S. pneumoniae pneumonia group had significantly higher Penh values compared to the uninfected controls. These data suggest that neonatal S. pneumoniae pneumonia promoted an aberrant ASM phenotype and AHR development in mice model.
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Tanaka, Akitaka, Shigeki Nakamura, Masafumi Seki, Kenji Fukudome, Naoki Iwanaga, Yoshifumi Imamura, Taiga Miyazaki et al. "Toll-Like Receptor 4 Agonistic Antibody Promotes Innate Immunity against Severe Pneumonia Induced by Coinfection with Influenza Virus and Streptococcus pneumoniae". Clinical and Vaccine Immunology 20, n. 7 (1 maggio 2013): 977–85. http://dx.doi.org/10.1128/cvi.00010-13.
Testo completoAbstract (sommario):
ABSTRACTCoinfection with bacteria is a major cause of mortality during influenza epidemics. Recently, Toll-like receptor (TLR) agonists were shown to have immunomodulatory functions. In the present study, we investigated the effectiveness and mechanisms of the new TLR4 agonistic monoclonal antibody UT12 against secondary pneumococcal pneumonia induced by coinfection with influenza virus in a mouse model. Mice were intranasally inoculated withStreptococcus pneumoniae2 days after influenza virus inoculation. UT12 was intraperitoneally administered 2 h before each inoculation. Survival rates were significantly increased and body weight loss was significantly decreased by UT12 administration. Additionally, the production of inflammatory mediators was significantly suppressed by the administration of UT12. In a histopathological study, pneumonia in UT12-treated mice was very mild compared to that in control mice. UT12 increased antimicrobial defense through the acceleration of macrophage recruitment into the lower respiratory tract induced by c-Jun N-terminal kinase (JNK) and nuclear factor kappaB (NF-κB) pathway-dependent monocyte chemoattractant protein 1 (MCP-1) production. Collectively, these findings indicate that UT12 promoted pulmonary innate immunity and may reduce the severity of severe pneumonia induced by coinfection with influenza virus andS. pneumoniae. This immunomodulatory effect of UT12 improves the prognosis of secondary pneumococcal pneumonia and makes UT12 an attractive candidate for treating severe infectious diseases.
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Muñoz, Natalia, Laurye Van Maele, Juan M. Marqués, Analía Rial, Jean-Claude Sirard e José A. Chabalgoity. "Mucosal Administration of Flagellin Protects Mice from Streptococcus pneumoniae Lung Infection". Infection and Immunity 78, n. 10 (19 luglio 2010): 4226–33. http://dx.doi.org/10.1128/iai.00224-10.
Testo completoAbstract (sommario):
ABSTRACT Streptococcus pneumoniae is a major cause of pneumonia in infants and the elderly. Innate defenses are essential to the control of pneumococcal infections, and deficient responses can trigger disease in susceptible individuals. Here we showed that flagellin can locally activate innate immunity and thereby increase the resistance to acute pneumonia. Flagellin mucosal treatment improved S. pneumoniae clearance in the lungs and promoted increased survival of infection. In addition, lung architecture was fully restored after the treatment of infected mice, indicating that flagellin allows the reestablishment of steady-state conditions. Using a flagellin mutant that is unable to signal through Toll-like receptor 5 (TLR5), we established that TLR5 signaling is essential for protection. In the respiratory tract, flagellin induced neutrophil infiltration into airways and upregulated the expression of genes coding for interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), CXCL1, CXCL2, and CCL20. Using depleting antibodies, we demonstrated that neutrophils are major effectors of protection. Further, we found that B- and T-cell-deficient SCID mice clear S. pneumoniae challenge to the same extent as immunocompetent animals, suggesting that these cell populations are not required for flagellin-induced protection. In conclusion, this study emphasizes that mucosal stimulation of innate immunity by a TLR not naturally engaged by S. pneumoniae can increase the potential to cure pneumococcal pneumonia.
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Jahan, Rownak, Shirin Tarafder e Anwarul Haque. "Aetiological ahents of Adult Bacterial Pneumonia parients admitted at a Tertiary Care Hospital in Dhaka city". Journal of Shaheed Suhrawardy Medical College 7, n. 1 (7 marzo 2017): 22–25. http://dx.doi.org/10.3329/jssmc.v7i1.31786.
Testo completoAbstract (sommario):
Background: Bacterial pneumonia is one of the most common causes of mortality and morbidity worldwide especially in adults.Objective: The purpose of this present study was to identify the aetiological agents and antimicrobial sensitivity pattern of bacterial pneumonia in patients admitted at intensive care unit (ICU).Methodology: This cross sectional study was carried out in the Department of Microbiology & Immunology at Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh from August 2012 to July 2013. Blood and tracheal aspirates (TA) culture were done in clinically diagnosed pneumonia patients admitted in the ICU of BSMMU. PCR of TA was performed to identify Legionella species. Urine ICT of patients was done to detect Streptococcus pneumoniae and Legionella pneumophila serogroup 1 antigens. Antimicrobial susceptibility of isolated bacteria was done by disc diffusion method.Result: A total of 36 pneumonia patients admitted at ICU were recruited. The most common identified bacteria were Acinetobacter species (33.3%) followed by Pseudomonas species (30.5%), Klebsiella pneumoniae (11.1%), Escherichia coli (5.5%), Enterobacter aerogenes (5.5%), Legionella (8.3%), Citrobacterfreundii (2.8%) and Proteus mirabilis (2.8%). Majority of the bacteria were resistant to first line antibiotics and highly sensitive to carbapenems.Conclusion: Most common isolated bacteria are the Acinetobacter species, Pseudomonas species and Klebsiella pneumoniae among the pneumonic patients with the resistant to first line antibiotics and sensitive to carbapenems.J Shaheed Suhrawardy Med Coll, 2015; 7(1):22-25
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Gubba, Siddeswar, Donald E. Low e James M. Musser. "Expression and Characterization of Group AStreptococcus Extracellular Cysteine Protease Recombinant Mutant Proteins and Documentation of Seroconversion during Human Invasive Disease Episodes". Infection and Immunity 66, n. 2 (1 febbraio 1998): 765–70. http://dx.doi.org/10.1128/iai.66.2.765-770.1998.
Testo completoAbstract (sommario):
ABSTRACT A recent study with isogenic strains constructed by recombinant DNA strategies unambiguously documented that a highly conserved extracellular cysteine protease expressed by Streptococcus pyogenes (group A Streptococcus [GAS]) is a critical virulence factor in a mouse model of invasive disease (S. Lukomski, S. Sreevatsan, C. Amberg, W. Reichardt, M. Woischnik, A. Podbielski, and J. M. Musser, J. Clin. Invest. 99:2574–2580, 1997). To facilitate further investigations of the streptococcal cysteine protease, recombinant proteins composed of a 40-kDa zymogen containing a C192S amino acid substitution that ablates enzymatic activity, a 28-kDa mature protein with the C192S replacement, and a 12-kDa propeptide were purified from Escherichia colicontaining His tag expression vectors. The recombinant C192S zymogen retained apparently normal structural integrity, as assessed by the ability of purified wild-type streptococcal cysteine protease to process the 40-kDa molecule to the 28-kDa mature form. All three recombinant purified proteins retained immunologic reactivity with polyclonal and monoclonal antibodies. Humans with a diverse range of invasive disease episodes (erysipelas, cellulitis, pneumonia, bacteremia, septic arthritis, streptococcal toxic shock syndrome, and necrotizing fasciitis) caused by six distinct M types of GAS seroconverted to the streptococcal cysteine protease. These results demonstrate that this GAS protein is expressed in vivo during the course of human infections and thereby provide additional evidence that the cysteine protease participates in host-pathogen interactions in some patients.
Tesi sul tema "Streptococcus pneumoniae – immunologie"
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Gomes, Machado Marina. "The role of acetate in macrophage`s response against Streptococcus pneumoniae". Thesis, Université de Lille (2022-....), 2022. https://pepite-depot.univ-lille.fr/LIBRE/EDBSL/2022/2022ULILS001.pdf.
Testo completoAbstract (sommario):
Les acides gras à chaîne courte (AGCC) sont des métabolites produits principalement par le microbiote intestinal. Ils jouent un rôle important dans la régulation des réponses immunitaires et inflammatoires. L'acétate, le principal AGCC, est décrit pour disséminer dans l’organisme et réguler la fonction d’organes distaux tels que les poumons. Des travaux récents indiquent une fonction dans le contrôle des agents pathogènes, notamment d’origine bactérienne. Notre groupe a précédemment démontré que l'acétate augmente l’élimination de Streptococcus pneumoniae dans le cadre d'une infection secondaire post-virale. Cette protection est médiée par les macrophages alvéolaires, la première ligne de défense pulmonaire. Ainsi, notre objectif était d'évaluer l'effet de l'acétate sur l’activité bactéricide des macrophages alvéolaires et d’identifier les mécanismes impliqués dans cette réponse. Nous montrons ici que la supplémentation en acétate dans l'eau de boisson module la sécrétion de protéines de défense par les cellules pulmonaires murines et conduit à une réduction de la charge de S. pneumoniae. Nous montrons par analyse transcriptomique (RNAseq) que l’acétate induit une signature spécifique de défense de l’hôte au sein des macrophages alvéolaires conditionnés en présence de S. pneumoniae. Cet effet s’accompagne par l’augmentation de l’activité bactéricide des macrophages mediée pour l'oxyde nitrique (NO). L’augmentation de NO induit par acétate dépendait de l'augmentation des niveaux d'IL-1β. De manière surprenante, la production d'IL-1β déclenchée par l'acétate est indépendante de son récepteur de surface (Free-Fatty Acid Receptor 2) et des enzymes responsables de son métabolisme (Acetyl-CoA Synthetases 1/2). En contrepartie, l'acétate a modulé le profil glycolytique des macrophages induisant l’activation de HIF-1α, qui aboutit à la transcription de l’IL-1β. De plus, l'augmentation de la sécrétion de l’IL-1β déclenchée par l'acétate reposait sur l'activation de l'inflammasome NLRP3. En conclusion, nous avons identifié un nouveau mécanisme conduisant à l’élimination des bactéries par les macrophages alvéolaires traité avec l’acétate. L'acétate augmente la production et la sécrétion d'IL-1β selon un mécanisme dépendant de l'axe glycolyse/HIF-1α et de NLRP3, respectivement. Par conséquent, des niveaux plus élevés d'IL-1β conduit à une augmentation de la production de NO et une meilleure activité bactéricide des macrophagesShort chain fatty acids (SCFAs) are metabolites produced mainly by the gut microbiota with a known role in immune regulation. Acetate, the major SCFA, is described to disseminate to distal organs such as the lungs. Moreover, the literature supports that acetate modulates inflammation and improves bacterial clearance. Our group has previously demonstrated that acetate improves Streptococcus pneumoniae clearance in the context of a secondary post-viral infection. This protection is mediated by alveolar macrophages, the first line of pulmonary immune defense. Thus, our aim was to evaluate the effect of acetate on the killing ability of alveolar macrophages and to delineate the mechanisms involved in this response. Here we show that acetate supplementation in drinking water modulated the secretion of host defense proteins by murine pulmonary cells and led to reduced S. pneumoniae loads in the lungs. To understand the mechanisms of bacterial clearance, alveolar macrophages were used. Transcriptomic analysis (RNAseq) revealed that acetate induced a specific signature of host defense in S. pneumoniae conditioned macrophages. This associates with the improved killing ability of acetate treated macrophages mediated by nitric oxide (NO) production. Increased NO concentration triggered by acetate was dependent on augmentation of IL-1β levels. Surprisingly, IL-1β production led by acetate was neither dependent on its cell surface receptor (Free-Fatty Acid Receptor 2), nor on the enzymes responsible for its metabolism (Acetyl-CoA Synthetase 1 and 2). Alternatively, acetate enhanced the glycolytic profile of macrophages resulting in greater HIF-1α activity which culminated in higher transcription of IL-1β. Moreover, the increased secretion of IL-1β triggered by acetate relied on NLRP3 inflammasome activation. In conclusion, we unravel a new mechanism of bacterial killing by acetate-activated macrophages. We show that acetate increased IL-1β production and secretion in a mechanism dependent on the axis glycolysis/HIF-1α and NLRP3, respectively. Consequently, higher levels of IL-1β resulted in augmented NO production and improved killing ability of alveolar macrophages
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Champagne, Marie-Eve. "Ré-infections avec Streptococcus pneumoniae : effet sur les réponses immunes innée et acquise lors d'une pneumonie à pneumocoque". Master's thesis, Université Laval, 2007. http://hdl.handle.net/20.500.11794/19368.
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Fani, Fereshteh. "Genomic analysis of B-lactam resistance mechanisms in « Streptococcus pneumoniae »". Thesis, Université Laval, 2013. http://www.theses.ulaval.ca/2013/29750/29750.pdf.
Testo completoAbstract (sommario):
Streptococcus pneumoniae est le pathogène bactérien le plus important des voies respiratoires (pneumonie, bronchite et otite moyenne) chez les adultes et les enfants. Cette bactérie est responsable d’une morbidité et une mortalité importantes. Bien que la pénicilline présente une activité contre de nombreux isolats de S. pneumoniae, la résistance à cet antibiotique est aujourd'hui, fréquemment rencontrés à la fois à l'hôpital et dans la communauté. La résistance à la pénicilline chez Streptococcus pneumoniae est causée par un bloc de gènes codant pour des versions altérées de protéines liant la pénicilline (PLP). Néanmoins, S. pneumoniae a également développé des mécanismes de résistance à la pénicilline indépendants des PLPs altérées. L'objectif principal de cette thèse était d’utiliser des approches génomiques pour comprendre le génotype et le phénotype de résistance aux ß-lactamines chez S. pneumoniae. Le travail présenté dans cette thèse a indiqué que des mutations dans les PLPs ne sont pas suffisantes pour obtenir une résistance de haut niveau à la pénicilline et au céfotaxime. Cette étude a indiqué également que la sélection de la résistance à la pénicilline chez S. pneumoniae peut impliquer l’acquisition de mutations conférant une tolérance à l’accumulation d’oxydants causée par les antibiotiques. Cette tolérance peut se traduire par une augmentation de la survie qui permet possiblement la sélection des déterminants majeurs de résistance tels que des mutations dans les PLPs. Dans le cas des souches cliniques résistantes à la pénicilline, nous présentons également un nouveau rôle pour une alpha-amylase cytoplasmique conférant une résistance modérée à la pénicilline en présence d'altération des PLPs. Par ailleurs, nos travaux sur la résistance au céfotaxime chez S. pneumoniae a permis la découverte de nouveaux gènes impliquées dans la résistance au céfotaxime, y compris les gènes spr1333, spr0981, spr1704 et spr1098 qui codent respectivement pour un peptidoglycan GlcNAc déacetylase, une glycosyltransférase, un transporteur ABC et une sortase. Nos travaux génomiques ont permis de découvrir de nouveaux gènes de résistance aux β-lactamines chez S. pneumoniae.Streptococcus pneumoniae is the most important bacterial pathogen of the respiratory tract (pneumonitis, bronchitis and otitis media) in adults and children resulting in significant morbidity and mortality. Although penicillin shows activity against many isolates of S. pneumoniae, resistance to this antibiotic is now frequently encountered, both at the hospital and in the community. Penicillin resistance in Streptococcus pneumoniae is mediated by a mosaic of genes encoding altered penicillin-binding proteins (PBPs). Nonetheless, S. pneumoniae has also developed non-PBP mechanisms implicated in penicillin resistance. The principal objective of this thesis was to use global sequencing approaches to understand ß-lactam resistance genotype and phenotype in S. pneumoniae. The work presented in this thesis indicated that mutations in PBPs are not sufficient to achieve high level resistance to penicillin and cefotaxime. This study also indicates that the selection of resistance to penicillin in S. pneumoniae involves the acquisition of mutations conferring tolerance to the antibiotic-induced accumulation of oxidants. This tolerance can translate into an increased survival that putatively enables the selection of major resistance determinants such as mutations in PBPs. In the case of clinical isolates, we also report a new role for a cytoplasmic alpha amylase in conferring moderate resistance to penicillin in the presence of altered PBPs. Furthermore, our works on cefotaxime resistance has allowed the discovery of novel cefotaxime resistance genes in S. pneumoniae including spr1333, spr0981, spr1704 and spr1098 coding respectively for a peptidoglycan GlcNAc deacetylase, a glycosyltransferase, an ABC transporter, and a sortase were implicated in resistance to cefotaxime. Our genomic approaches were useful to discover novel β-lactam resistance genes in S. pneumoniae.
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Heming, Nicholas. "Rôle protecteur du récepteur FcαRl (CD89) dans la pneumopathie à Streptococcus pneumoniae". Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC264.
Testo completoAbstract (sommario):
Les immunoglobulines jouent un rôle clé dans l'interaction hôte-pathogène. Les immunoglobulines A (IgA) sous forme d'IgA sécrétoires sont en particulier impliquées dans la défense des épithéliums pulmonaire et digestif. Le FcaRI (ou CD89) est un récepteur spécifique liant la fraction Fc des IgA qui est responsable de l'activité biologique de ces immunoglobulines. Une fois lié à son ligand, le FcaRI transmet un signal intracellulaire via l'adaptateur Fcy qui est porteur d'un motif ITAM (Immunoreceptor tyrosine-based activation motif) sur sa portion intra cellulaire. L'adaptateur Fcy est également capable de transduire un signal inhibiteur dénommé ITAM inhibiteur (ITAMi). Nous montrons ici que le Streptococcus pneumoniae est capable de lier directement (sans opsonine) le FcaRI recombinant, à la fois en solution et in vitro, et que cette interaction est inhibée par l'adjonction de FcaRI soluble recombinant. Nous avons également montré que l'adjonction de Streptococcus pneumoniae sur des macrophages transgéniques pour le FcaRI induit une activation cellulaire et une production de cytokines pro inflammatoires. Dans une seconde partie nous avons démontré que, dans un modèle murin de pneumopathie à Streptococcus pneumoniae, la présence de FcaRI constitue un avantage de survie. Cette dernière est associée à une diminution des lésions histologiques pulmonaires et une moindre invasion bactérienne pulmonaire. Au final nous concluons que la famille des Fc récepteurs est capable de lier des pathogènes de manière indépendante des opsonines. Le FcaRI pourrait ainsi avoir une fonction supplémentaire en agissant comme un senseur antibactérienAn innate immune response is essential for survival of the host upon infection. Opsonin-independent bacteria recognition for tell activation is an important mechanism for bacteria clearance. Here, we show that the IgA receptor FcaRI binds Streptococcus pneumoniae directly, independently of IgA and mediates immunoreceptor tyrosine-based activation motif (ITAMa) signaling. These interactions increased bacteria phagocytosis and cytokine release and induced reactive oxygen species production by bone marrow-derived macrophages from FcaRI-transgenic mice. In these mice, using two differen models of sepsis, the presence of FcaRI was associated with host protection as evidenced by enhanced local bacterial containment, decreased tissue damage and increased survival. This work reveals the significant involvement of the ITAM-bearing FcaRI in innate immunity
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Thiriot, Aude. "Identification et caractérisation, grâce aux lignées de souris dérivées d'individus sauvages, d'une nouvelle population de lymphocytes B conservée dans le genre Mus : les cellules Bw". Paris 6, 2008. http://www.theses.fr/2008PA066673.
Testo completoAbstract (sommario):
L'utilisation de lignées de souris dérivées d’individus sauvages nous a permis d’identifier une nouvelle sous-population de lymphocytes B, nommée "Bw", qui se distingue par de nombreux critères des sous-populations de cellules B déjà connues chez la souris. Alors que la présence des cellules B-1a CD5pos est quasiment restreinte aux lignées de souris appartenant à la sous-espèce Mus musculus domesticus, les lymphocytes Bw sont conservés à travers l’évolution du genre Mus. Les souris de laboratoire ont hérité la population B-1a CD5pos de la sous-espèce M. M. Domesticus. Les lymphocytes Bw péritonéaux présentent le phénotype caractéristique suivant : CD19posCD5negMac-1posB220highIgMhighIgDhighCD43negCD9neg. Les cellules Bw sont retrouvées, à des fréquences variables dans la rate, les ganglions, la cavité péritonéale ainsi que les PBL. Le répertoire anticorps de ces lymphocytes est enrichi en spécificités autoréactives contre des antigènes tels que l’ADN, la tubuline ou l’actine, ainsi qu’envers des globules rouges traités par de la broméline. En réponse au LPS et au CpG, ligands des TLR 4 et 9 respectivement, les cellules Bw produisent plus d’anticorps anti-PC que les cellules B-2. Il en est de même suite à une immunisation par la bactérie S. Pneumoniae. Les précurseurs issus de la moelle osseuse sont capables, au même titre que les précurseurs foetaux, de se différencier en cellules Bw, contrairement aux précurseurs des cellules B-1 qui sont enrichis dans le foie foetal. Ce travail révèle la présence d’une nouvelle population de cellules B Mac-1pos, les lymphocytes Bw, conservée à travers l’évolution du genre Mus et impliquée dans des réponses immunitaires innées.
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Parameswar, Archana R. "Towards development of a fully synthetic conjugate vaccine investigation of structural analogs of Streptococcus pneumoniae serogroup 6 /". Diss., St. Louis, Mo. : University of Missouri--St. Louis, 2008. http://etd.umsl.edu/r3161.
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Alsharif, Sultan M. M. "Stress response and pathogenicity in Streptococcus pneumoniae". Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5231/.
Testo completoAbstract (sommario):
The pathogen Streptococcus pneumoniae encounters different levels of oxygen during the infection cycle including colonisation, pneumonia, bateraemia and meningitis. These different anatomical niches require high levels of genome changes to sense and respond to those external environmental stimuli. The bacterial gene expression is known to be affected by oxygen, and it must react properly for survival and for developing invasive pneumococcal desiseases (IPDs). Microarray techniques have allowed scanning the whole pneumococcal genome during growth in different tensions of oxygen mimicking in vivo conditions. It was found that oxygenated growth conditions have significantly elevated several key virulence genes. This was further confirmed with qRT-PCR for a selection of genes implicated in pathogenicity. Moreover, post-transcriptional stages have been also investigated such as protein production, biofilm formation, biological activities and adherence assays for several virulence factors performed under the effect of presence or absence of oxygen. The data illustrate that 420 out of 2,236 genes (17 % of the entire TIGR4 genome) were differentially expressed in the presence of oxygen compared to its absence. 262 genes (11 %) were over-expressed when pneumococci were grown in oxygenated conditions relative to transcriptional profile in anaerobic growth conditions, indicating the magnitude of roles played by oxygen on pneumococcal gene expression. Anaerobic growth of TIGR4 showed down-regulation of 158 genes (7 %). Oxygen modulates induction of ply, pspC and other seven genes involved in pili structuring subunits (rlrA, rrgA, rrgB and rrgC) and assembling enzymes (srtB, srtC and srtD). This may suggest that the pneumococcal population grown under atmospheric environment is equipped with greater capability to progress IPDs compared to anaerobically grown bacteria. In addition to this, pneumococcal adhesion in vitro for TIGR4 grown in oxygenated or anaerobic growth conditions revealed a significant increase in those grown in oxygenated growth conditions, indicating that oxygen may play a key role in bacterial-host attachment. Interestingly, ablation of pspC has resulted in similar adhesion percentages of TIGR4 grown under both conditions, oxygenated and anaerobic. Furthermore, several genes involved in metabolism were up-regulated in oxygenated environment, particularly transporters, which are considered highly important for a bacterium that lacks an electron transport chain, catalase and tricarboxylic acid. Additionally, the results showed phenotypic characterisation and changes in cells morphology from pneumococcal growth curves for several strainswith different genome backgrounds grown under different levels of oxygen concentrations. Further investigation of the pathogen biology revealed differences in pneumolysin production and activity. These findings highlight that virulence genes expression is induced once the micro-organism is exposed to oxygenated environment, and data analysis has demonstrated potential links between pneumococcal metabolism and their ability to cause diseases.
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Gauthier, Jean-François. "Rôle des peptides n-formylés et des chimiokines dans le recrutement neutrophilique lors d'une pneumonie à pneumocoque". Thesis, Université Laval, 2007. http://www.theses.ulaval.ca/2007/24278/24278.pdf.
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Lee, Katherine Shi-Hui. "The host immune response to Streptococcus pneumoniae : bridging innate and adaptive immunity /". Download the dissertation in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/lee2006.pdf.
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Thompson, Rebecca. "Polyreactive and antigen-specific B-cell response to Streptococcus pneumoniae". University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1334150627.
Testo completoLibri sul tema "Streptococcus pneumoniae – immunologie"
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Life with the pneumococcus: Notes from the bedside, laboratory, and library. Philadelphia: University of Pennsylvania Press, 1985.
Cerca il testo completoCapitoli di libri sul tema "Streptococcus pneumoniae – immunologie"
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Humann, Jessica, Kim LeMessurier e Elaine Tuomanen. "Streptococcus pneumoniae: The Prototype of Lung Responses in Pneumonia". In Mucosal Immunology of Acute Bacterial Pneumonia, 213–38. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5326-0_9.
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Sestini, P., L. Nencioni, L. Villa, D. Boraschi e A. Tagliabue. "Antibacterial Activity Against Streptococcus Pneumoniae by Mouse Lung Lymphocytes". In Recent Advances in Mucosal Immunology, 517–25. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5344-7_61.
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Richards, James C., e Malcolm B. Perry. "Structural Comparisons of Streptococcus Pneumoniae Specific Polysaccharides of Group 9 (9N, 9V, 9L, 9A) Related to the Choice of Vaccine Components". In The Molecular Immunology of Complex Carbohydrates, 593–94. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_21.
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Richards, James C., Malcolm B. Perry e M. Moreau. "Elucidation and Comparison of the Chemical Structures of the Specific Capsular Polysaccharides of Streptococcus Pneumoniae Groups 11 (11F, 11B, 11C, And 11A)". In The Molecular Immunology of Complex Carbohydrates, 595–96. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_22.
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Richards, James C., e Malcolm B. Perry. "Application of Two Dimensional NMR Methods to the Structural Elucidation of Complex Polysaccharide Antigens. The Structure of the Capsular Polysaccharide of Streptococcus Pneumoniae Type 22 F". In The Molecular Immunology of Complex Carbohydrates, 597–98. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1663-3_23.
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