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Journal articles on the topic 'Parasites – Immunologie'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Greenwood, B. M. "Parasite Immunology and the clinical immunologist." Parasite Immunology 23, no. 10 (2001): 517. http://dx.doi.org/10.1046/j.1365-3024.2001.00413.x.

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2

POULIN, R. "Relative infection levels and taxonomic distances among the host species used by a parasite: insights into parasite specialization." Parasitology 130, no. 1 (2004): 109–15. http://dx.doi.org/10.1017/s0031182004006304.

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Parasites often exploit more than one host species at any stage in their life-cycle, but the extent to which these host species are used varies greatly. Parasites typically achieve their highest prevalence, intensity and/or abundance in one host species (the principal host), whereas infection levels in auxiliary hosts range from relatively high to very low. The present study examines what influences the distribution of parasite individuals among their different host species, using metazoan parasites that use freshwater fish as their definitive or only host. Specifically, I test the hypothesis

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3

Kim, Ju Yeong, Myung-Hee Yi, and Tai-Soon Yong. "Allergen-like Molecules from Parasites." Current Protein & Peptide Science 21, no. 2 (2020): 186–202. http://dx.doi.org/10.2174/1389203720666190708154300.

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Parasite infections modulate immunologic responses, and the loss of parasite infections in the last two to three decades might explain the increased prevalence of allergic diseases in developed countries. However, parasites can enhance allergic responses. Parasites contain or release allergen-like molecules that induce the specific immunoglobulin, IgE, and trigger type-2 immune responses. Some parasites and their proteins, such as Anisakis and Echinococcus granulosus allergens, act as typical allergens. A number of IgE-binding proteins of various helminthic parasites are cross-reactive to othe

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Duneau, David, and Dieter Ebert. "The role of moulting in parasite defence." Proceedings of the Royal Society B: Biological Sciences 279, no. 1740 (2012): 3049–54. http://dx.doi.org/10.1098/rspb.2012.0407.

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Parasitic infections consist of a succession of steps during which hosts and parasites interact in specific manners. At each step, hosts can use diverse defence mechanisms to counteract the parasite's attempts to invade and exploit them. Of these steps, the penetration of parasites into the host is a key step for a successful infection and the epithelium is the first line of host defence. The shedding of this protective layer (moulting) is a crucial feature in the life cycle of several invertebrate and vertebrate taxa, and is generally considered to make hosts vulnerable to parasites and preda

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5

McRobert, Louisa, Peter Preiser, Sarah Sharp, et al. "Distinct Trafficking and Localization of STEVOR Proteins in Three Stages of the Plasmodium falciparum Life Cycle." Infection and Immunity 72, no. 11 (2004): 6597–602. http://dx.doi.org/10.1128/iai.72.11.6597-6602.2004.

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ABSTRACT The genome of Plasmodium falciparum harbors three extensive multigene families, var, rif, and stevor (for subtelomeric variable open reading frame), located mainly in the subtelomeric regions of the parasite's 14 chromosomes. STEVOR variants are known to be expressed in asexual parasites, but no function has as yet been ascribed to this protein family. We have examined the expression of STEVOR proteins in intraerythrocytic sexual stages, gametocytes, and extracellular sporozoites isolated from infected Anopheles mosquitoes. In gametocytes, stevor transcripts appear transiently early i

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6

KOEHLER, ANSON V., and ROBERT POULIN. "Clone-specific immune reactions in a trematode-crustacean system." Parasitology 139, no. 1 (2011): 128–36. http://dx.doi.org/10.1017/s0031182011001739.

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SUMMARYVariability of immune responses is an essential aspect of ecological immunology, yet how much of this variability is due to differences among parasite genotypes remains unknown. Here, variation in immune response of the crab, Macrophthalmus hirtipes, is examined as a function of experimental exposure to 10 clonal cercarial lineages of the trematode Maritrema novaezealandensis. Our goals were (1) to assess the variability of the host immune reaction elicited by 10 parasite clones, (2) to test if the heterozygosity–fitness correlation, whereby organisms with higher heterozygosities achiev

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7

Hofmeester, Tim R., Esther J. Bügel, Bob Hendrikx, et al. "Parasite Load and Site-Specific Parasite Pressure as Determinants of Immune Indices in Two Sympatric Rodent Species." Animals 9, no. 12 (2019): 1015. http://dx.doi.org/10.3390/ani9121015.

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Wildlife is exposed to parasites from the environment. This parasite pressure, which differs among areas, likely shapes the immunological strategies of animals. Individuals differ in the number of parasites they encounter and host, and this parasite load also influences the immune system. The relative impact of parasite pressure vs. parasite load on different host species, particularly those implicated as important reservoirs of zoonotic pathogens, is poorly understood. We captured bank voles (Myodes glareolus) and wood mice (Apodemus sylvaticus) at four sites in the Netherlands. We sampled su

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8

Chen, Xian-Ming, Steven P. O'Hara, Bing Q. Huang, et al. "Apical Organelle Discharge by Cryptosporidium parvum Is Temperature, Cytoskeleton, and Intracellular Calcium Dependent and Required for Host Cell Invasion." Infection and Immunity 72, no. 12 (2004): 6806–16. http://dx.doi.org/10.1128/iai.72.12.6806-6816.2004.

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ABSTRACT The apical organelles in apicomplexan parasites are characteristic secretory vesicles containing complex mixtures of molecules. While apical organelle discharge has been demonstrated to be involved in the cellular invasion of some apicomplexan parasites, including Toxoplasma gondii and Plasmodium spp., the mechanisms of apical organelle discharge by Cryptosporidium parvum sporozoites and its role in host cell invasion are unclear. Here we show that the discharge of C. parvum apical organelles occurs in a temperature-dependent fashion. The inhibition of parasite actin and tubulin polym

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9

TURNER, A. K., P. M. BELDOMENICO, K. BOWN, et al. "Host–parasite biology in the real world: the field voles of Kielder." Parasitology 141, no. 8 (2014): 997–1017. http://dx.doi.org/10.1017/s0031182014000171.

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SUMMARYResearch on the interactions between the field voles (Microtus agrestis) of Kielder Forest and their natural parasites dates back to the 1930s. These early studies were primarily concerned with understanding how parasites shape the characteristic cyclic population dynamics of their hosts. However, since the early 2000s, research on the Kielder field voles has expanded considerably and the system has now been utilized for the study of host–parasite biology across many levels, including genetics, evolutionary ecology, immunology and epidemiology. The Kielder field voles therefore represen

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10

Persson, Catrine M., Henrik Lambert, Polya P. Vutova, et al. "Transmission of Toxoplasma gondii from Infected Dendritic Cells to Natural Killer Cells." Infection and Immunity 77, no. 3 (2009): 970–76. http://dx.doi.org/10.1128/iai.00833-08.

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ABSTRACT The obligate intracellular parasite Toxoplasma gondii can actively infect any nucleated cell type, including cells from the immune system. In the present study, we observed that a large number of natural killer (NK) cells were infected by T. gondii early after intraperitoneal inoculation of parasites into C57BL/6 mice. Interestingly, one mechanism of NK cell infection involved NK cell-mediated targeting of infected dendritic cells (DC). Perforin-dependent killing of infected DC led to active egress of infectious parasites that rapidly infected adjacent effector NK cells. Infected NK c

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11

Brown, Wendy C. "Parasite immunology." Veterinary Immunology and Immunopathology 35 (February 1993): 176–90. http://dx.doi.org/10.1016/0165-2427(93)90148-w.

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12

Dong, Xiaojuan, Ghada H. Abdelnabi, Sung H. Lee, et al. "Enhanced Egress of Intracellular Eimeria tenella Sporozoites by Splenic Lymphocytes from Coccidian-Infected Chickens." Infection and Immunity 79, no. 8 (2011): 3465–70. http://dx.doi.org/10.1128/iai.01334-10.

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ABSTRACTEgress, which describes the mechanism that some intracellular parasites use to exit from parasitophorous vacuoles and host cells, plays a very important role in the parasite life cycle and is central toEimeriapropagation and pathogenesis. Despite the importance of egress in the intracellular parasite's life cycle, very little information is known on this process compared to other steps, e.g., invasion. The present study was conducted to investigate the interplay between the host adaptive immune system andEimeriaegression. Splenic lymphocytes or soluble immune factors were incubated wit

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13

Fernandez, Victor, Marcel Hommel, Qijun Chen, Per Hagblom, and Mats Wahlgren. "Small, Clonally Variant Antigens Expressed on the Surface of the Plasmodium falciparum–Infected Erythrocyte Are Encoded by the rif Gene Family and Are the Target of Human Immune Responses." Journal of Experimental Medicine 190, no. 10 (1999): 1393–404. http://dx.doi.org/10.1084/jem.190.10.1393.

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Disease severity in Plasmodium falciparum infections is a direct consequence of the parasite's efficient evasion of the defense mechanisms of the human host. To date, one parasite-derived molecule, the antigenically variant adhesin P. falciparum erythrocyte membrane protein 1 (PfEMP1), is known to be transported to the infected erythrocyte (pRBC) surface, where it mediates binding to different host receptors. Here we report that multiple additional proteins are expressed by the parasite at the pRBC surface, including a large cluster of clonally variant antigens of 30–45 kD. We have found these

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14

Morley, N. J., J. W. Lewis, and D. Hoole. "Pollutant-induced effects on immunological and physiological interactions in aquatic host–trematode systems: implications for parasite transmission." Journal of Helminthology 80, no. 2 (2006): 137–49. http://dx.doi.org/10.1079/joh2006345.

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AbstractUnder conditions of pollution both host and parasite are susceptible to the pathogenic effects of toxicants, which in turn may result in detrimental changes to their immunological and physiological processes. Digenetic trematodes, which encompass species of both medical and economic importance, possess complex life cycles and are common parasites of both vertebrates and molluscs. The combined stress induced by pollution and parasitism influences the physiology of the host which can have implications not only on host survival but also on the functional biology of resident parasite popul

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15

Grainger, John R., Katie A. Smith, James P. Hewitson та ін. "Helminth secretions induce de novo T cell Foxp3 expression and regulatory function through the TGF-β pathway". Journal of Experimental Medicine 207, № 11 (2010): 2331–41. http://dx.doi.org/10.1084/jem.20101074.

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Foxp3-expressing regulatory T (T reg) cells have been implicated in parasite-driven inhibition of host immunity during chronic infection. We addressed whether parasites can directly induce T reg cells. Foxp3 expression was stimulated in naive Foxp3− T cells in mice infected with the intestinal helminth Heligmosomoides polygyrus. In vitro, parasite-secreted proteins (termed H. polygyrus excretory-secretory antigen [HES]) induced de novo Foxp3 expression in fluorescence-sorted Foxp3− splenocytes from Foxp3–green fluorescent protein reporter mice. HES-induced T reg cells suppressed both in vitro

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16

Manning-Cela, Rebeca, Arantxa Cortés, Elena González-Rey, Wesley C. Van Voorhis, John Swindle, and Antonio González. "LYT1 Protein Is Required for Efficient In Vitro Infection by Trypanosoma cruzi." Infection and Immunity 69, no. 6 (2001): 3916–23. http://dx.doi.org/10.1128/iai.69.6.3916-3923.2001.

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ABSTRACT Trypanosoma cruzi invasion of host cells involves several discrete steps: attachment, parasite internalization mediated by recruitment and fusion of host cell lysosomes, and escape from the parasitophorous vacuole to liberate amastigotes to multiply freely in the cytosol. This report describes the initial characterization of theLYT1 gene and the demonstration that the gene product is involved in cell lysis and infectivity. Mutational analysis demonstrated that deletion of LYT1 resulted in attenuation of infection, which was associated with diminished hemolytic activity. Reintroduction

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17

Simpson, S. J. "IMMUNOLOGY: Primed by Parasites." Science 311, no. 5761 (2006): 579d—581d. http://dx.doi.org/10.1126/science.311.5761.579d.

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18

Berger, Chloé Suzanne, and Nadia Aubin-Horth. "The secretome of a parasite alters its host's behaviour but does not recapitulate the behavioural response to infection." Proceedings of the Royal Society B: Biological Sciences 287, no. 1925 (2020): 20200412. http://dx.doi.org/10.1098/rspb.2020.0412.

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Parasites with complex life cycles have been proposed to manipulate the behaviour of their intermediate hosts to increase the probability of reaching their final host. The cause of these drastic behavioural changes could be manipulation factors released by the parasite in its environment (the secretome), but this has rarely been assessed. We studied a non-cerebral parasite, the cestode Schistocephalus solidus , and its intermediate host, the threespine stickleback ( Gasterosteus aculeatus ), whose response to danger becomes significantly diminished when infected. These altered behaviours appea

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19

Blythe, Jane E., Xue Yan Yam, Claudia Kuss, et al. "Plasmodium falciparum STEVOR Proteins Are Highly Expressed in Patient Isolates and Located in the Surface Membranes of Infected Red Blood Cells and the Apical Tips of Merozoites." Infection and Immunity 76, no. 7 (2008): 3329–36. http://dx.doi.org/10.1128/iai.01460-07.

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ABSTRACT The human parasite Plasmodium falciparum has the potential to express a vast repertoire of variant proteins on the surface of the infected red blood cell (iRBC). Variation in the expression pattern of these proteins is linked to antigenic variation and thereby evasion of host antibody-mediated immunity. The genes in the stevor multigene family code for small variant antigens that are expressed in blood-stage parasites where they can be detected in membranous structures called Maurer's clefts (MC). Some studies have indicated that STEVOR protein may also be trafficked to the iRBC membr

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20

Pauwels, Kevin, Luc De Meester, Ellen Decaestecker, and Robby Stoks. "Phenoloxidase but not lytic activity reflects resistance against Pasteuria ramosa in Daphnia magna." Biology Letters 7, no. 1 (2010): 156–59. http://dx.doi.org/10.1098/rsbl.2010.0634.

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The field of ecological immunology strongly relies on indicators of immunocompetence. Two major indicators in invertebrates, the activity of phenoloxidase (PO) and lytic activity have recently been questioned in studies showing that, across a natural range of baseline levels, these indicators did not predict resistance against a manipulated challenge with natural parasites. We confirmed this finding by showing that baseline levels of PO and lytic activity in the host Daphnia magna were not related to spore load of the parasite Pasteuria ramosa . Yet, PO levels in infected hosts did predict spo

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21

Park, A. W. "Food web structure selects for parasite host range." Proceedings of the Royal Society B: Biological Sciences 286, no. 1908 (2019): 20191277. http://dx.doi.org/10.1098/rspb.2019.1277.

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Complex life cycle parasites, including helminths, use intermediate hosts for development and definitive hosts for reproduction, with interactions between the two host types governed by food web structure. I study how a parasite's intermediate host range is controlled by the diet breadth of definitive host species and the cost of parasite generalism, a putative fitness cost that assumes host range trades off against fitness derived from a host species. In spite of such costs, a benefit to generalism may occur when the definitive host exhibits a large diet breadth, enhancing transmission of gen

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22

Ferrante, Antonio. "Parasite Immunology Symposium." International Journal for Parasitology 27, no. 2 (1997): 181. http://dx.doi.org/10.1016/s0020-7519(96)00142-7.

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23

Conrad, Sean M., Dalit Strauss-Ayali, Ann E. Field, Matthias Mack, and David M. Mosser. "Leishmania-Derived Murine Monocyte Chemoattractant Protein 1 Enhances the Recruitment of a Restrictive Population of CC Chemokine Receptor 2-Positive Macrophages." Infection and Immunity 75, no. 2 (2006): 653–65. http://dx.doi.org/10.1128/iai.01314-06.

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ABSTRACT Transgenic Leishmania parasites that encode the murine chemokine monocyte chemoattractant protein 1 (MCP-1) were generated. These parasites transcribed MCP-1 mRNA and secreted MCP-1 protein. Infection of BALB/c, C57BL/6, or MCP-1 knockout (KO) mice with these parasites resulted in minimal lesion development with fewer parasites in the infected foot, lymph node, and spleen compared to wild-type-infected mice. In contrast, transgenic parasites caused substantial lesions with relatively high numbers of parasites in CC chemokine receptor 2 (CCR2) KO mice, indicating that the parasites are

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Sultan, Ali A., Vandana Thathy, Victor Nussenzweig, and Robert Ménard. "Green Fluorescent Protein as a Marker in Plasmodium berghei Transformation." Infection and Immunity 67, no. 5 (1999): 2602–6. http://dx.doi.org/10.1128/iai.67.5.2602-2606.1999.

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ABSTRACT We present a new marker that confers both resistance to pyrimethamine and green fluorescent protein-based fluorescence on the malarial parasite Plasmodium berghei. A single copy of the cassette integrated into the genome is sufficient to direct fluorescence in parasites throughout the life cycle, in both its mosquito and vertebrate hosts. Erythrocyte stages of the parasite that express the marker can be sorted from control parasites by flow cytometry. Pyrimethamine pressure is not necessary for maintaining the cassette in transformed parasites during their sporogonic cycle in mosquito

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Nair, Sethu C., Carrie F. Brooks, Christopher D. Goodman, et al. "Apicoplast isoprenoid precursor synthesis and the molecular basis of fosmidomycin resistance in Toxoplasma gondii." Journal of Experimental Medicine 208, no. 7 (2011): 1547–59. http://dx.doi.org/10.1084/jem.20110039.

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Apicomplexa are important pathogens that include the causative agents of malaria, toxoplasmosis, and cryptosporidiosis. Apicomplexan parasites contain a relict chloroplast, the apicoplast. The apicoplast is indispensable and an attractive drug target. The apicoplast is home to a 1-deoxy-d-xylulose-5-phosphate (DOXP) pathway for the synthesis of isoprenoid precursors. This pathway is believed to be the most conserved function of the apicoplast, and fosmidomycin, a specific inhibitor of the pathway, is an effective antimalarial. Surprisingly, fosmidomycin has no effect on most other apicomplexan

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Versteeg, Leroy, Mashal M. Almutairi, Peter J. Hotez, and Jeroen Pollet. "Enlisting the mRNA Vaccine Platform to Combat Parasitic Infections." Vaccines 7, no. 4 (2019): 122. http://dx.doi.org/10.3390/vaccines7040122.

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Despite medical progress, more than a billion people still suffer daily from parasitic infections. Vaccination is recognized as one of the most sustainable options to control parasitic diseases. However, the development of protective and therapeutic vaccines against tropical parasites has proven to be exceptionally challenging for both scientific and economic reasons. For certain parasitic diseases, traditional vaccine platforms are not well-suited, due to the complexity of the parasite life cycles and the parasite’s ability to evade the human immune system. An effective anti-parasite vaccine

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27

Ozwara, Hastings, Jan A. M. Langermans, Clemens H. M. Kocken, et al. "Transfected Plasmodium knowlesi Produces Bioactive Host Gamma Interferon: a New Perspective for Modulating Immune Responses to Malaria Parasites." Infection and Immunity 71, no. 8 (2003): 4375–81. http://dx.doi.org/10.1128/iai.71.8.4375-4381.2003.

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ABSTRACT Transgenic pathogenic microorganisms expressing host cytokines such as gamma interferon (IFN-γ) have been shown to manipulate host-pathogen interaction, leading to immunomodulation and enhanced protection. Expression of host cytokines in malaria parasites offers the opportunity to investigate the potential of an immunomodulatory approach by generating immunopotentiated parasites. Using the primate malaria parasite Plasmodium knowlesi, we explored the conditions for expressing host cytokines in malaria parasites. P. knowlesi parasites transfected with DNA constructs for expressing rhes

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Brittingham, Andrew, Gang Chen, Bradford S. McGwire, Kwang-Poo Chang, and David M. Mosser. "Interaction of Leishmania gp63 with Cellular Receptors for Fibronectin." Infection and Immunity 67, no. 9 (1999): 4477–84. http://dx.doi.org/10.1128/iai.67.9.4477-4484.1999.

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ABSTRACT The most abundant protein on the surface of the promastigote form of the protozoan parasites Leishmania spp. is a 63-kDa molecule, designated gp63 or leishmanolysin. Because gp63 has been shown to possess fibronectin-like properties, we examined the interaction of gp63 with the cellular receptors for fibronectin. We measured the direct binding of Leishmania to human macrophages or to transfected mammalian cells expressing human fibronectin receptors. Leishmania expressing gp63 exhibited modest but reproducible adhesion to human macrophages and to transfected CHO cells expressing α4/β1

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Phelps, Eric D., Kristin R. Sweeney, and Ira J. Blader. "Toxoplasma gondii Rhoptry Discharge Correlates with Activation of the Early Growth Response 2 Host Cell Transcription Factor." Infection and Immunity 76, no. 10 (2008): 4703–12. http://dx.doi.org/10.1128/iai.01447-07.

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ABSTRACT Toxoplasma gondii is a ubiquitous apicomplexan parasite that can cause severe disease in fetuses and immune-compromised patients. Rhoptries, micronemes, and dense granules, which are secretory organelles unique to Toxoplasma and other apicomplexan parasites, play critical roles in parasite growth and virulence. To understand how these organelles modulate infected host cells, we sought to identify host cell transcription factors triggered by their release. Early growth response 2 (EGR2) is a host cell transcription factor that is rapidly upregulated and activated in Toxoplasma-infected

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Fairhurst, Rick M., Hisashi Fujioka, Karen Hayton, Kathleen F. Collins, and Thomas E. Wellems. "Aberrant development of Plasmodium falciparum in hemoglobin CC red cells: implications for the malaria protective effect of the homozygous state." Blood 101, no. 8 (2003): 3309–15. http://dx.doi.org/10.1182/blood-2002-10-3105.

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Abstract Although selection of hemoglobin C (HbC) by malaria has been speculated for decades, only recently have epidemiologic studies provided support for HbC protection against malaria in West Africa. A reduced risk of malaria associated with the homozygous CC state has been attributed to the inability of CC cells to support parasite multiplication in vitro. However, there have been conflicting data and conclusions regarding the ability of CC red cells to support parasite replication. Reports that parasites cannot multiply in CC cells in vitro contrast with detection of substantial parasite

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Bei, Amy K., Ababacar Diouf, Kazutoyo Miura, et al. "Immune Characterization of Plasmodium falciparum Parasites with a Shared Genetic Signature in a Region of Decreasing Transmission." Infection and Immunity 83, no. 1 (2014): 276–85. http://dx.doi.org/10.1128/iai.01979-14.

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As the intensity of malaria transmission has declined,Plasmodium falciparumparasite populations have displayed decreased clonal diversity resulting from the emergence of many parasites with common genetic signatures (CGS). We have monitored such CGS parasite clusters from 2006 to 2013 in Thiès, Senegal, using the molecular barcode. The first, and one of the largest observed clusters of CGS parasites, was present in 24% of clinical isolates in 2008, declined to 3.4% of clinical isolates in 2009, and then disappeared. To begin to explore the relationship between the immune responses of the popul

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Roulin, Alexandre, Martin W. G. Brinkhof, Pierre Bize, et al. "Which chick is tasty to parasites? The importance of host immunology vs. parasite life history." Journal of Animal Ecology 72, no. 1 (2003): 75–81. http://dx.doi.org/10.1046/j.1365-2656.2003.00677.x.

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Rajendran, Esther, Morgan Clark, Cibelly Goulart, et al. "Substrate-mediated regulation of the arginine transporter of Toxoplasma gondii." PLOS Pathogens 17, no. 8 (2021): e1009816. http://dx.doi.org/10.1371/journal.ppat.1009816.

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Intracellular parasites, such as the apicomplexan Toxoplasma gondii, are adept at scavenging nutrients from their host. However, there is little understanding of how parasites sense and respond to the changing nutrient environments they encounter during an infection. TgApiAT1, a member of the apicomplexan ApiAT family of amino acid transporters, is the major uptake route for the essential amino acid L-arginine (Arg) in T. gondii. Here, we show that the abundance of TgApiAT1, and hence the rate of uptake of Arg, is regulated by the availability of Arg in the parasite’s external environment, inc

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Bloom, Barry R. "Immunology of bacteria and parasites." Immunology Today 10, no. 12 (1989): 397–99. http://dx.doi.org/10.1016/0167-5699(89)90032-7.

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Ma, Ji Su, Miwa Sasai, Jun Ohshima, et al. "Selective and strain-specific NFAT4 activation by the Toxoplasma gondii polymorphic dense granule protein GRA6." Journal of Experimental Medicine 211, no. 10 (2014): 2013–32. http://dx.doi.org/10.1084/jem.20131272.

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Toxoplasma gondii infection results in co-option and subversion of host cellular signaling pathways. This process involves discharge of T. gondii effector molecules from parasite secretory organelles such as rhoptries and dense granules. We report that the T. gondii polymorphic dense granule protein GRA6 regulates activation of the host transcription factor nuclear factor of activated T cells 4 (NFAT4). GRA6 overexpression robustly and selectively activated NFAT4 via calcium modulating ligand (CAMLG). Infection with wild-type (WT) but not GRA6-deficient parasites induced NFAT4 activation. More

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Moore, J. M., N. Kumar, L. D. Shultz, and T. V. Rajan. "Maintenance of the human malarial parasite, Plasmodium falciparum, in scid mice and transmission of gametocytes to mosquitoes." Journal of Experimental Medicine 181, no. 6 (1995): 2265–70. http://dx.doi.org/10.1084/jem.181.6.2265.

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The study of human malaria has been hampered by the lack of small animal models for the human-infecting malarial parasites. To approach this problem, the erythrocytic stages of the human malarial parasite Plasmodium falciparum were adapted to in vitro growth in the presence of ascites fluid from mice homozygous for the severe-combined immunodeficiency (scid) mutation. Human red blood cells (hRBCs) infected with these adapted parasites were then injected i.p. into nonobese diabetic scid/scid (NOD/LtSz-scid) mice. With daily supplemental intraperitoneal boosts of uninfected hRBCs, parasites were

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Gregg, Beth, Betsy C. Taylor, Beena John, et al. "Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts." Infection and Immunity 81, no. 5 (2013): 1635–43. http://dx.doi.org/10.1128/iai.01126-12.

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ABSTRACTNatural infection byToxoplasma gondiioccurs via oral ingestion of tissue cysts that rupture in the small intestine, releasing zoites that infect locally before disseminating throughout the host. The studies presented here used fluorescent parasites combined with flow cytometry and multiphoton microscopy techniques to understand the events associated with parasite replication in the mucosa. At 3 days postinfection with tissue cysts, parasites were localized in small foci and flow cytometry revealed parasites present in macrophages, neutrophils, and monocytes in the lamina propria. By da

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Ezenwa, Vanessa O., Elizabeth A. Archie, Meggan E. Craft, et al. "Host behaviour–parasite feedback: an essential link between animal behaviour and disease ecology." Proceedings of the Royal Society B: Biological Sciences 283, no. 1828 (2016): 20153078. http://dx.doi.org/10.1098/rspb.2015.3078.

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Animal behaviour and the ecology and evolution of parasites are inextricably linked. For this reason, animal behaviourists and disease ecologists have been interested in the intersection of their respective fields for decades. Despite this interest, most research at the behaviour–disease interface focuses either on how host behaviour affects parasites or how parasites affect behaviour, with little overlap between the two. Yet, the majority of interactions between hosts and parasites are probably reciprocal, such that host behaviour feeds back on parasites and vice versa. Explicitly considering

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Pastrana, Diana V., Nithyakalyani Raghavan, Peter FitzGerald, et al. "Filarial Nematode Parasites Secrete a Homologue of the Human Cytokine Macrophage Migration Inhibitory Factor." Infection and Immunity 66, no. 12 (1998): 5955–63. http://dx.doi.org/10.1128/iai.66.12.5955-5963.1998.

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ABSTRACT Filarial nematode parasites establish long-term chronic infections in the context of an antiparasite immunity that is strongly biased toward a Th2 response. The mechanisms that lead to this Th2 bias toward filarial antigens are not clear, but one possibility is that the parasites produce molecules that have the capacity to proactively modify their immunological environment. Here we report that filarial parasites of humans secrete a homologue of the human proinflammatory cytokine macrophage migration inhibitory factor (MIF) that has the capability of modifying the activity of human mon

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Tewari, Rita, Solabomi A. Ogun, Ruwani S. Gunaratne, Andrea Crisanti, and Anthony A. Holder. "Disruption of Plasmodium berghei merozoite surface protein 7 gene modulates parasite growth in vivo." Blood 105, no. 1 (2005): 394–96. http://dx.doi.org/10.1182/blood-2004-06-2106.

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Abstract Merozoite invasion of red blood cells is crucial to the development of the parasite that causes malaria. Merozoite surface proteins (MSPs) mediate the first interaction between parasite and erythrocyte. In Plasmodium falciparum, they include a complex of products from at least 3 genes (msp1, msp6, and msp7), one of which, msp7, is part of a gene family containing 3 and 6 adjacent members in Plasmodium yoelii and Plasmodium falciparum, respectively. We have identified and disrupted msp7 in the Plasmodium berghei gene family. The protein is expressed in schizonts and colocalizes with MS

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Roth, E. Jr, V. Joulin, S. Miwa, et al. "The use of enzymopathic human red cells in the study of malarial parasite glucose metabolism." Blood 71, no. 5 (1988): 1408–13. http://dx.doi.org/10.1182/blood.v71.5.1408.1408.

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Abstract The in vitro growth of Plasmodium falciparum malaria parasites was assayed in mutant red cells deficient in either diphosphoglycerate mutase (DPGM) or phosphoglycerate kinase (PGK). In addition, cDNA probes developed for human DNA sequences coding for these enzymes were used to examine the parasite genome by means of restriction endonuclease digestion and Southern blot analysis of parasite DNA. In both types of enzymopathic red cells, parasite growth was normal. In infected DPGM deficient red cells, no DPGM activity could be detected, and in normal red cells, DPGM activity declined sl

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Roth, E. Jr, V. Joulin, S. Miwa, et al. "The use of enzymopathic human red cells in the study of malarial parasite glucose metabolism." Blood 71, no. 5 (1988): 1408–13. http://dx.doi.org/10.1182/blood.v71.5.1408.bloodjournal7151408.

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The in vitro growth of Plasmodium falciparum malaria parasites was assayed in mutant red cells deficient in either diphosphoglycerate mutase (DPGM) or phosphoglycerate kinase (PGK). In addition, cDNA probes developed for human DNA sequences coding for these enzymes were used to examine the parasite genome by means of restriction endonuclease digestion and Southern blot analysis of parasite DNA. In both types of enzymopathic red cells, parasite growth was normal. In infected DPGM deficient red cells, no DPGM activity could be detected, and in normal red cells, DPGM activity declined slightly in

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Málaga, Sergio, and Nobuko Yoshida. "Targeted Reduction in Expression ofTrypanosoma cruzi Surface Glycoprotein gp90 Increases Parasite Infectivity." Infection and Immunity 69, no. 1 (2001): 353–59. http://dx.doi.org/10.1128/iai.69.1.353-359.2001.

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ABSTRACT A previous study had shown that the expression of gp90, a stage-specific surface glycoprotein of Trypanosoma cruzimetacyclic trypomastigotes, is inversely correlated with the parasite's ability to invade mammalian cells. By using antisense oligonucleotides complementary to a region of the gp90 gene implicated in host cell adhesion, we investigated whether the selective inhibition of gp90 synthesis affected the capacity of metacyclic forms to enter target cells. Parasites were incubated for 24 h with 20 μM PS1, a phosphorothioate oligonucleotide based on a sequence of the gp90 coding s

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Tadiri, Christina P., Marilyn E. Scott, and Gregor F. Fussmann. "Microparasite dispersal in metapopulations: a boon or bane to the host population?" Proceedings of the Royal Society B: Biological Sciences 285, no. 1885 (2018): 20181519. http://dx.doi.org/10.1098/rspb.2018.1519.

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Although connectivity can promote host species persistence in a metapopulation, dispersal may also enable disease transmission, an effect further complicated by the impact that parasite distribution may have on host–parasite population dynamics. We investigated the effects of connectivity and initial parasite distribution (clustered or dispersed) on microparasite–host dynamics in experimental metapopulations, using guppies and Gyrodactylus turnbulli . We created metapopulations of guppies divided into four subpopulations and introduced either a low level of parasites to all subpopulations (dis

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Strauss, Alexander T., Jessica L. Hite, David J. Civitello, Marta S. Shocket, Carla E. Cáceres, and Spencer R. Hall. "Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission." Proceedings of the Royal Society B: Biological Sciences 286, no. 1915 (2019): 20192164. http://dx.doi.org/10.1098/rspb.2019.2164.

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Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequently contradict this assumption. General yet mechanistic models can explain why transmission depends nonlinearly on parasite density and thereby identify potential defensive strategies of hosts. For example, hosts could decrease their exposure rates at higher parasite densities (via behavioural avoidance) or decrease their per-parasite susceptibility when encountering more parasites (e.g. via stronger immune responses). To illustrate, we fitted mechani

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Coetzer, Theresa L., and Dewaldt Engelbrecht. "To Each His Own: Fever Induces Different Suicide Mechanisms in Early and Late Stage Plasmodium falciparum Malaria Parasites in vitro." Blood 122, no. 21 (2013): 3427. http://dx.doi.org/10.1182/blood.v122.21.3427.3427.

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Abstract Malaria is characterised by cyclical febrile episodes that result from the rupture of mature schizont-infected erythrocytes releasing merozoites. In patients infected with Plasmodium falciparum, fever may reach peak temperatures as high as 41°C, last for 2-6 hours and recur every 48 hours, in accordance with the parasite life cycle. Febrile episodes typically have a deleterious effect on parasites, and probably benefit the host by aiding parasite clearance; however, a reduction in parasitemia may also be an advantage for the parasite by limiting the burden of infection on the host and

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Fairlie, W. Douglas, Tim P. Spurck, Joanne E. McCoubrie, et al. "Inhibition of Malaria Parasite Development by a Cyclic Peptide That Targets the Vital Parasite Protein SERA5." Infection and Immunity 76, no. 9 (2008): 4332–44. http://dx.doi.org/10.1128/iai.00278-08.

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ABSTRACT The serine repeat antigen (SERA) proteins of the malaria parasites Plasmodium spp. contain a putative enzyme domain similar to that of papain family cysteine proteases. In Plasmodium falciparum parasites, more than half of the SERA family proteins, including the most abundantly expressed form, SERA5, have a cysteine-to-serine substitution within the putative catalytic triad of the active site. Although SERA5 is required for blood-stage parasite survival, the occurrence of a noncanonical catalytic triad casts doubt on the importance of the enzyme domain in this function. We used phage

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Onyiche, ThankGod E., Keisuke Suganuma, Ikuo Igarashi, Naoaki Yokoyama, Xuenan Xuan, and Oriel Thekisoe. "A Review on Equine Piroplasmosis: Epidemiology, Vector Ecology, Risk Factors, Host Immunity, Diagnosis and Control." International Journal of Environmental Research and Public Health 16, no. 10 (2019): 1736. http://dx.doi.org/10.3390/ijerph16101736.

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Equine Piroplasmosis (EP) is a tick-borne disease caused by apicomplexan protozoan parasites, Babesia caballi and Theileria equi. The disease is responsible for serious economic losses to the equine industry. It principally affects donkeys, horses, mules, and zebra but DNA of the parasites has also been detected in dogs and camels raising doubt about their host specificity. The disease is endemic in tropical and temperate regions of the world where the competent tick vectors are prevalent. Infected equids remain carrier for life with T. equi infection, whilst, infection with B. caballi is clea

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O'Donnell, Aidan J., Kimberley F. Prior, and Sarah E. Reece. "Host circadian clocks do not set the schedule for the within-host replication of malaria parasites." Proceedings of the Royal Society B: Biological Sciences 287, no. 1932 (2020): 20200347. http://dx.doi.org/10.1098/rspb.2020.0347.

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Circadian clocks coordinate organisms' activities with daily cycles in their environment. Parasites are subject to daily rhythms in the within-host environment, resulting from clock-control of host activities, including immune responses. Parasites also exhibit rhythms in their activities: the timing of within-host replication by malaria parasites is coordinated to host feeding rhythms. Precisely which host feeding-related rhythm(s) parasites align with and how this is achieved are unknown. Understanding rhythmic replication in malaria parasites matters because it underpins disease symptoms and

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Crilly, Nathan P., and Monica R. Mugnier. "Thinking outside the blood: Perspectives on tissue-resident Trypanosoma brucei." PLOS Pathogens 17, no. 9 (2021): e1009866. http://dx.doi.org/10.1371/journal.ppat.1009866.

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Trypanosoma brucei is a protozoan parasite that causes human and animal African trypanosomiases (HAT and AAT). In the mammalian host, the parasite lives entirely extracellularly, in both the blood and interstitial spaces in tissues. Although most T. brucei research has focused on the biology of blood- and central nervous system (CNS)-resident parasites, a number of recent studies have highlighted parasite reservoirs in the dermis and adipose tissue, leading to a renewed interest in tissue-resident parasite populations. In light of this renewed interest, work describing tissue-resident parasite

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