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Cp Wilkes - One of the best experts on this subject based on the ideXlab platform.
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An attempt to artificially select Strongyloides ratti for resistance to the Host Immune Response.
Parasite immunology, 2004Co-Authors: Cp Wilkes, Mark VineyAbstract:SUMMARY Previous work has selected Heligmosomoides polygyrus for increased survival and reproduction in Hosts with prior exposure to H. polygyrus, and therefore ‘Immune’ to this parasite. We investigated whether Strongyloides ratti would respond similarly to selection for survival and reproduction in S. ratti-Immune Hosts. During 32 generations of selection, there appeared to be an initial, brief Response to this selection, but this was not sustained and, eventually, the Immune-selected line died out. Specific measures of the Response to selection at generations 6, 12 and 25 did not detect any significant Response to selection. Therefore, we have failed to select a line of S. ratti for increased resistance to its Host Immune Response.
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The effect of the Host Immune Response on the parasitic nematode Strongyloides ratti.
Parasitology, 2004Co-Authors: Cp Wilkes, F J Thompson, M P Gardner, S Paterson, M E VineyAbstract:The Host Immune Response has profound effects on parasitic nematode infections. Here we have investigated how a range of infection parameters are affected by Host Immune Responses and by their suppression and enhancement. The infection parameters considered were the number of parasitic females, their size, per capita fecundity and intestinal position. We found that in immunosuppressive treatments worms persist in the gut, sometimes with a greater per capita fecundity, maintain their size and have a more anterior gut position, compared with worms from control animals. In immunization treatments there are fewer worms in the gut, sometimes with a lower per capita fecundity and they are shorter and have a more posterior gut position, compared with worms from control animals. Worms from animals immunosuppressed by corticosteroid treatment reverse their changes in size and gut position. This description of these phenomena pave the way for a molecular biological analysis of how these changes in infection parameters are brought about by the Host Immune Response.
Mark Viney - One of the best experts on this subject based on the ideXlab platform.
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An attempt to artificially select Strongyloides ratti for resistance to the Host Immune Response.
Parasite immunology, 2004Co-Authors: Cp Wilkes, Mark VineyAbstract:SUMMARY Previous work has selected Heligmosomoides polygyrus for increased survival and reproduction in Hosts with prior exposure to H. polygyrus, and therefore ‘Immune’ to this parasite. We investigated whether Strongyloides ratti would respond similarly to selection for survival and reproduction in S. ratti-Immune Hosts. During 32 generations of selection, there appeared to be an initial, brief Response to this selection, but this was not sustained and, eventually, the Immune-selected line died out. Specific measures of the Response to selection at generations 6, 12 and 25 did not detect any significant Response to selection. Therefore, we have failed to select a line of S. ratti for increased resistance to its Host Immune Response.
Juliet V. Spencer - One of the best experts on this subject based on the ideXlab platform.
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Viral manipulation of the Host Immune Response
Current opinion in immunology, 2015Co-Authors: Allison F. Christiaansen, Steven M. Varga, Juliet V. SpencerAbstract:Viruses are obligate intracellular parasites that require a Host for essential machinery to replicate and ultimately be transmitted to new susceptible Hosts. At the same time, the Immune system has evolved to protect the human body from invasion by viruses and other pathogens. To counter this, viruses have developed an arsenal of strategies to not only avoid Immune detection but to actively manipulate Host Immune Responses to create an environment more favorable for infection. Here, we describe recent advances uncovering novel mechanisms by which viruses skew Host Immune Responses through modulation of cytokine and chemokine signaling networks, interference with antigen presentation and T cell Responses, and preventing antibody production.
Vishukumar Aimanianda - One of the best experts on this subject based on the ideXlab platform.
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The glycobiology of fungal cell wall polysaccharides and its relation in Host Immune Response
2018Co-Authors: Sarah S. W. Wong, Vishukumar Aimanianda, Jean-paul LatgéAbstract:Objective: Aspergillus fumigatus is a ubiquitous fungal pathogen that can cause a wide range of infections, for example, invasive pulmonary aspergillosis (IPA) and allergic bronchopulmonary aspergillosis (ABPA). IPA was previously observed to mainly occur among immunocompromised populations, however, in recent years, more cases have been observed in otherwise immunocompetent patients. Therefore, it is important to elucidate the relationship between the fungal pathogen and the Host Immune system. In addition, in ABPA patients, other underlying pulmonary conditions are usually concurrently present, which challenge the normal clearance mechanism of conidia by phagocytes. As a result, the conidia are allowed to swell and germinate. Dormant conidia possess a layer of rodlet and melanin that masks the underneath polysaccharides in the cell wall. As the conidia swell, this outer layer disappears and the cell wall polysaccharides are exposed and are free to interact with the Host Immune system. Polysaccharides have been considered immunogenic. But the relationship between the glycobiology and Host Immune Response is not well studied. In this study, the aim is to examine the effect of the length, linkage and solubility of galactomannan and alpha-1,3-glucan with the Host Immune Response. Methods: Galactomannan oligosaccharides of different length and linkage and alpha-1,3-glucan oligosaacharides were synthesized. Native polysaccharides of galactomannan and alpha-1,3-glucan are also extracted from the A. fumigatus mycelia. All the oligosaccharides and native polysaccharides were immobilized or directly inoculated to microtite plates with PBMCs isolated from healthy donors. The stimulation was performed in the presence or absence of normal human serum, to investigate the significance of soluble mediators. The supernatant was collected after 24-h incubation and stored at -20C for further analysis of the cytokine induction. Results: The degree of cytokine induction is directly proportional to the length of both galactomannan and alpha-1,3-glucan. The short oligosaccharides and the native polysaccharides display several differences. The short oligosaccharides have to be immobilized (that is, insoluble, since free short oligosaccharides are soluble) and provided with serum for stimulation of cytokine production, while the native polysaccharides do not have to be immobilized and serum is not required. Conclusion: The length and solubility of cell wall polysaccharides are important factors in modulation the cytokine induction. Humoral Immune factors, such as soluble mediators, may play a significant role in the recognition of short oligosaccharides, but not for the longer counterpart. Taken together, there exists a link between the glycobiology of A. fumigatus cell wall polysaccharides and the Host Immune Response.
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Fungal melanin stimulates surfactant protein D–mediated opsonization of and Host Immune Response to Aspergillus fumigatus spores
Journal of Biological Chemistry, 2018Co-Authors: Sarah Sze Wah Wong, Manjusha Rani, Eswari Dodagatta-marri, Taruna Madan, Uday Kishore, Oumaïma Ibrahim-granet, Arvind Sahu, Jean-paul Latgé, Jagadeesh Bayry, Vishukumar AimaniandaAbstract:Surfactant protein D (SP-D), a C-type lectin and pattern-recognition soluble factor, plays an important role in Immune surveillance to detect and eliminate human pulmonary pathogens. SP-D has been shown to protect against infections with the most ubiquitous airborne fungal pathogen, Aspergillus fumigatus, but the fungal surface component(s) interacting with SP-D is unknown. Here, we show that SP-D binds to melanin pigment on the surface of A. fumigatus dormant spores (conidia). SP-D also exhibited an affinity to two cell-wall polysaccharides of A. fumigatus, galactomannan (GM) and galactosaminogalactan (GAG). The immunolabeling pattern of SP-D was punctate on the conidial surface and was uniform on germinating conidia, in accordance with the localization of melanin, GM, and GAG. We also found that the collagen-like domain of SP-D is involved in its interaction with melanin, whereas its carbohydrate-recognition domain recognized GM and GAG. Unlike un-opsonized conidia, SP-D-opsonized conidia were phagocytosed more efficiently and stimulated the secretion of proinflammatory cytokines by human monocyte-derived macrophages. Furthermore, SP-D-/- mice challenged intranasally with wildtype conidia or melanin gHosts (i.e. hollow melanin spheres) displayed significantly reduced proinflammatory cytokines in the lung compared with wildtype mice. In summary, SP-D binds to melanin present on the dormant A. fumigatus conidial surface, facilitates conidial phagocytosis, and stimulates the Host Immune Response.
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Fungal melanin stimulates surfactant protein D-mediated opsonization of and Host Immune Response to Aspergillus fumigatus spores
Journal of Biological Chemistry, 2018Co-Authors: Sarah Sze Wah Wong, Manjusha Rani, Eswari Dodagatta-marri, Taruna Madan, Uday Kishore, Oumaïma Ibrahim-granet, Arvind Sahu, Jean-paul Latgé, Jagadeesh Bayry, Vishukumar AimaniandaAbstract:Surfactant protein D (SP-D), a C-type lectin and pattern-recognition soluble factor, plays an important role in Immune surveillance to detect and eliminate human pulmonary pathogens. SP-D has been shown to protect against infections with the most ubiquitous airborne fungal pathogen, Aspergillus fumigatus, but the fungal surface component(s) interacting with SP-D is unknown. Here, we show that SP-D binds to melanin pigment on the surface of A. fumigatus dormant spores (conidia). SP-D also exhibited an affinity to two cell-wall polysaccharides of A. fumigatus, galactomannan (GM) and galactosaminogalactan (GAG). The immunolabeling pattern of SP-D was punctate on the conidial surface and was uniform on germinating conidia, in accordance with the localization of melanin, GM, and GAG. We also found that the collagen-like domain of SP-D is involved in its interaction with melanin, whereas its carbohydrate-recognition domain recognized GM and GAG. Unlike un-opsonized conidia, SP-D-opsonized conidia were phagocytosed more efficiently and stimulated the secretion of proinflammatory cytokines by human monocyte-derived macrophages. Furthermore, SP-D(-/-) mice challenged intranasally with wildtype conidia or melanin gHosts (i.e. hollow melanin spheres) displayed significantly reduced proinflammatory cytokines in the lung compared with wildtype mice. In summary, SP-D binds to melanin present on the dormant A. fumigatus conidial surface, facilitates conidial phagocytosis, and stimulates the Host Immune Response.
Csaba Szabo - One of the best experts on this subject based on the ideXlab platform.
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h2s a bacterial defense mechanism against the Host Immune Response
Infection and Immunity, 2018Co-Authors: Tracy Toliverkinsky, Weihua Cui, Gabor Toro, Seungjin Lee, Konstantin Shatalin, Evgeny Nudler, Csaba SzaboAbstract:ABSTRACT The biological mediator hydrogen sulfide (H 2 S) is produced by bacteria and has been shown to be cytoprotective against oxidative stress and to increase the sensitivity of various bacteria to a range of antibiotic drugs. Here we evaluated whether bacterial H 2 S provides resistance against the Immune Response, using two bacterial species that are common sources of nosocomial infections, Escherichia coli and Staphylococcus aureus. Elevations in H 2 S levels increased the resistance of both species to Immune-mediated killing. Clearances of infections with wild-type and genetically H 2 S-deficient E. coli and S. aureus were compared in vitro and in mouse models of abdominal sepsis and burn wound infection. Also, inhibitors of H 2 S-producing enzymes were used to assess bacterial killing by leukocytes. We found that inhibition of bacterial H 2 S production can increase the susceptibility of both bacterial species to rapid killing by Immune cells and can improve bacterial clearance after severe burn, an injury that increases susceptibility to opportunistic infections. These findings support the role of H 2 S as a bacterial defense mechanism against the Host Response and implicate bacterial H 2 S inhibition as a potential therapeutic intervention in the prevention or treatment of infections.