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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Parasitic Diseases Laboratory » Research » Publications at this Location » Publication #332453

Research Project: Detection and Control of Foodborne Parasites for Food Safety

Location: Animal Parasitic Diseases Laboratory

Title: Developmental profile of select immune cells in mice infected with Trichinella spiralis during the intestinal phase

Author
item Ding, J - CHINESE CENTER FOR DISEASE CONTROL
item Bai, X - JILIN UNIVERSITY
item Wang, Xl - JILIN UNIVERSITY
item Wang, Yf - CHINESE CENTER FOR DISEASE CONTROL
item Shi, Hn - MASSACHUSETTS GENERAL HOSPITAL
item Rosenthal, Benjamin
item Boireau, Pascal - FRENCH AGENCY FOR FOOD, ENVIRONMENTAL AND OCCUPATIONAL HEALTH & SAFETY (ANSES)
item Wu, Xp - CHINESE CENTER FOR DISEASE CONTROL
item Liu, My - JILIN UNIVERSITY
item Liu, Xl - CHINESE CENTER FOR DISEASE CONTROL

Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/10/2016
Publication Date: 11/15/2016
Citation: Ding, J., Bai, X., Wang, X., Wang, Y., Shi, H., Rosenthal, B.M., Boireau, P., Wu, X., Liu, M., Liu, X. 2016. Developmental profile of select immune cells in mice infected with Trichinella spiralis during the intestinal phase. Veterinary Parasitology. 231: 77-82.

Interpretive Summary: Trichinella parasites cause foodborne illness when their larvae are ingested in contaminated meat and, in the intestine, subsequently develop into adults, mate, and give birth to a next generation of larvae. How the parasite supresses immunity long enough to ensure successful reproduction remains uncertain, and examining this process has implications not only for the devlopment of vaccines against this disease, but also sheds light on how immunity in the gut is regulated more generally. Here, we showed that this parasite can induce several mechanisms for suppressing the immune responses in the intestine, including by distorting the composition of T cells, by increasing the occurrence of T cell suppressor cells, and by downregulating expression of markers on macrophages that would otherwise induce prolifferation of protective immune cell populations. Taken together, these results will interest parasitologists, immunologists, and others interested in the means by which parasitic infection can influence homeostatis and immune function.

Technical Abstract: Trichinella spiralis can cause immunosuppression during the intestinal phase of early infection. However, changes in the peripheral blood during T. spiralis early infection remain unclear. Here, select immune cells in mice infected with 500 muscle larvae (ML) of T. spiralis during the intestinal phase of infection were studied. First, the recovery rates of the intestinal worms and female fecundity were determined, and the results showed that the intestinal worms were completely eliminated at 17 days post-infection (dpi) and that large numbers of new-born larvae (NBL) were generated from 5 to 9 dpi. Using flow cytometry, it was shown that the number of CD4+ T cells and CD8+ T cells increased over the entire intestinal phase, except on 7 dpi when CD4+ T cells decreased significantly compared to the control groups. Although both CD4+ and CD8+ T cells increased, CD8+ T cells increased more than CD4+ T cells, leading to a lower CD4+/CD8+ ratio compared to the control group. Subsequently, a depression of the proliferative response of T cells to concanavalin A (Con A) was noticed at 7 and 11 dpi. Although the proliferative response of B cells to LPS was enhanced, the number of B cells from mouse peripheral blood stimulated by T. spiralis antigens showed no differences with the control group prior to 11 dpi. The expression of CD14 on monocyte-macrophages decreased during the same period, which meant that the antigen-presenting response was reduced in the immune system of the infected mice. Moreover, the alternatively activated macrophages were induced in T. spiralis early infection. These data provide a better understanding of the development of the intestinal immune response in mice infected with T. spiralis.