Abstract

Trichinellosis is a food-borne zoonotic parasitic disease that causes serious harm to human health and the pig breeding industry. However, there are reports that Trichinella spiralis (T. spiralis) infection can treat autoimmune diseases, including enteritis and experimental autoimmune encephalitis (EAE). However, research on the mechanism of T. spiralis infection in infectious enteritis has not been fully elucidated. Therefore, this experiment used Citrobacter rodentium (C. rodentium) to induce colitis in mouse models and explored its underlying mechanisms. In this experiment, a total of 72 C57BL/6 mice were randomly divided into four groups. Experimental mice in the TS and TS + CR groups were orally inoculated with individual T. spiralis larvae. At 21 days postinfection (dpi) with T. spiralis, experimental animals in the CR and TS + CR groups were inoculated by orogastric gavage with C. rodentium. The control group received PBS only. The results indicated that the weight loss and macroscopic and microscopic colon damage of mice in the TS + CR group were significantly decreased compared with those observed in the CR group. The results of flow cytometry showed that the expression levels of IL-4, IL-10 and CD4+CD25+Foxp3+ Tregs were increased (P < 0.05), while the expression levels of IFN-γ, IL-12 and IL-17 were decreased in the spleens and MLNs of the TS + CR experimental mice compared with the colitis model mice. ELISA results revealed that the TS + CR group not only elicited a strong IgG1 response (P < 0.01) but also a low level of IgG2a response (P < 0.05) relative to the CR group. The above results demonstrated that prior exposure of mice to T. spiralis infection ameliorated the severity of C. rodentium-induced infectious colitis.

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