Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease (CD), are chronic autoimmune diseases with a high recurrence rate. Epidemiological data have shown that the incidence of IBD increases annually because of improved sanitary conditions and reduced parasitic infection rates. In this experiment, experimental colitis was induced in mice by administering 2,4,6-trinitrobenzene sulfonic acid (TNBS) 28 days after they were infected with Trichinella spiralis to confirm that T. spiralis infection could alleviate the severity of TNBS-induced colitis. Thirty-six male BALB/c mice aged 6-8 weeks were randomly divided into four groups: control group (with 50% ethanol, Control), T. spiralis-infected group (TS-Control), TNBS-induced colitis model group (Colitis), and T. spiralis-pre-infected and TNBS-induced colitis group (TS-Colitis). The mice were sacrificed 3, 7, and 14 days after the model was established. Changes in various colitis indicators to investigate the effect of T. spiralis infection on TNBS-induced murine CD model. Results showed that the weight, DAI score, and macroscopic and microscopic colon damage in the TS-Colitis significantly decreased compared with those in the Colitis. ELISA revealed that the IFN-γ expression decreased and the IL-4 expression increased in the TS-Colitis compared with those in the Colitis. Western Blotting results revealed that the NF-κB expression increased in the Colitis and higher than those in the TS-Colitis. And Flow cytometry results revealed that the percentage of CD4+CD25+Foxp3+ Treg cells significantly increased in the TS-Colitis. T. spiralis-infected mice induced Th2 immune responses and balanced Th1 immune responses stimulated by TNBS to ameliorate intestinal inflammation.
Keywords: Immunoregulation; Inflammatory bowel disease; Trichinella spiralis.
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