Inflammatory bowel disease (IBD) is an inflammatory disease caused by the activity of effector immune cells, such as the overproduction of inflammatory cytokines. Helminth immunomodulation in the host has been shown to have therapeutic implications in IBD. In the present study, we investigated whether Metagonimus miyatai infection could ameliorate inflammatory diseases. Mice were infected with M. miyatai, and colitis was then induced through oral administration of dextran sulfate sodium (DSS). Weight loss, stool consistency, gross bleeding, colon length, and tissue inflammation were assessed by macroscopic and microscopic examinations. In addition, regulatory cytokine expression was observed in colon tissue by reverse transcription polymerase chain reaction. The results showed that M. miyatai infection decreased the clinical severity of DSS-induced colitis, including weight loss, bloody diarrhea, shortening of the colon, and colon tissue damage in mice (p < .05). The expression levels of tumor necrosis factor-α, interleukin-1b, and cyclooxygenase-2 in mice infected with helminth were lower than those in DSS-treated mice without helminthic infection (p < .05). The results of the research showed that pre-infection with M. miyatai ameliorated DSS-induced colitis in mice and may be a novel therapeutic strategy for the treatment of immunological diseases.
Keywords: Dextran sulfate sodium; Helminth; Metagonimus miyatai; Ulcerative colitis.
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