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Updated: Jun 4, 2026

Using Eggs from Schistosoma mansoni as an In vivo Model of Helminth-induced Lung Inflammation
Published on: June 5, 2012
Triggering receptor expressed on myeloid cells (TREM)-1 participates in Schistosoma mansoni inflammatory responses
1Institute of Tropical Medicine, National Yang-Ming University, Taipei, Taiwan.
Abstract:
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.
Insights
This study shows triggering receptor expressed on myeloid cells-1 (TREM-1) increases during Schistosoma mansoni infection in mice. However, parasite eggs may suppress TREM-1, potentially reducing the inflammatory response.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Inflammatory responses are amplified by triggering receptor expressed on myeloid cells-1 (TREM-1).
- Limited research exists on TREM-1's role in macrophage activation during parasitic infections.
Purpose of the Study:
- To investigate the role of TREM-1 in the Schistosoma mansoni infection model across early and chronic phases.
- To analyze TREM-1 expression on myeloid cells and its regulation by parasite components.
Main Methods:
- Flow cytometry to assess TREM-1 protein expression on CD11b(+) myeloid cells.
- Real-time PCR to measure TREM-1 mRNA levels in splenic and liver tissues.
- Stimulation of J774A.1 macrophage cell line with Schistosoma egg antigen.
Main Results:
- TREM-1 protein and mRNA expression gradually increased in splenic myeloid cells, peaking at 5 weeks post-infection.
- TREM-1 mRNA expression in liver tissue remained unchanged throughout infection.
- Schistosoma egg antigen inhibited TREM-1 expression on macrophages.
Conclusions:
- TREM-1 plays a role in the immune response to Schistosoma mansoni infection.
- Schistosoma eggs may downregulate TREM-1 expression, modulating the host's inflammatory response.
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