Triggering receptor expressed on myeloid cells (TREM)‐1 participates in Schistosoma mansoni inflammatory responses
Summary Inflammatory responses to microbial products are amplified by a pathway mediated by triggering a receptor expressed on the myeloid cells (TREM)‐1. Relatively a few studies have been performed to investigate the role of TREM‐1 in macrophage activation in response to parasitic infection. In th...
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Published in | Parasite immunology Vol. 33; no. 5; pp. 276 - 286 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.05.2011
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Subjects | |
Online Access | Get full text |
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Summary: | Summary
Inflammatory responses to microbial products are amplified by a pathway mediated by triggering a receptor expressed on the myeloid cells (TREM)‐1. Relatively a few studies have been performed to investigate the role of TREM‐1 in macrophage activation in response to parasitic infection. In this study, we delineate the role of the innate immunoreceptor TREM‐1 in the parasite Schistosoma mansoni infection model from early to late (chronic) phases of infection. Flow cytometry analysis revealed gradual increase in the production of TREM‐1 protein on CD11b+ myeloid cells, with maximum production at 5 weeks p.i. Similar results in the pattern of TREM‐1 mRNA expressions in splenic CD11b+ cells from infected mice were obtained by real‐time PCR. However, unlike in spleen, the TREM‐1 mRNA expression in liver tissue showed no significant increase throughout the infection, including periods of maximum production of parasite eggs. Administration of schistosoma egg homogenate antigen to stimulate J774A.1 cells inhibited TREM‐1 expression on the surface, indicating that some substances of the Schistosma eggs may inhibit the expression of TREM‐1 on macrophages, lowering the macrophage‐mediated inflammatory response of infected hosts. |
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Bibliography: | Disclosures: The authors do not have a commercial or other association that might pose a conflict of interest. The research of this manuscript has no financial support from any company that might benefit from the publication. These authors contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0141-9838 1365-3024 |
DOI: | 10.1111/j.1365-3024.2011.01284.x |