Schistosoma Japonicum Peptide SJMHE1 Inhibits Acute And Chronic Colitis Induced By Dextran Sulphate Sodium In Mice

Abstract Background: Harnessing helminth-based immunoregulation is a novel therapeutic strategy for many immune dysfunction disorders, including inflammatory bowel diseases. We previously identified a small-molecule peptide from Schistosoma japonicum and named it SJMHE1. SJMHE1 can suppress delayed-type hypersensitivity, collagen-induced arthritis, and asthma in mice. In this study, we assessed the effects of SJMHE1 on dextran sulfate sodium (DSS)-induced acute and chronic colitis. Methods: C57BL/6 mice were induced acute and chronic colitis by DSS, and were injected by emulsifier SJMHE1 or PBS. Then the mice were examined body weight loss, disease activity index, colon lengths, histopathology change, cytokine expression and helper T (Th) cell subset distribution.Results: We found that SJMHE1 treatment significantly suppressed DSS-induced acute and chronic colitis, improved disease activity and colon pathological damage. SJMHE1 treatment modulated the expression of pro-inflammatory and anti-inflammatory cytokines in splenocytes and the colon. Furthermore, SJMHE1 treatment reduced the percentage of Th1 and Th17 cells and increased the percentage of Th2 and regulatory T (Treg) cells in the splenocytes and mesenteric lymph nodes (MLNs) from mice with acute colitis. Similarly, SJMHE1 treatment upregulated the expression of IL-10 mRNA, and downregulated the expression of IL-17 mRNA, and modulated the Th cell balance in mice with chronic colitis. Conclusions: Our data show that SJMHE1 provided protection against acute and chronic colitis by restoring immune balance. As a small molecule, SJMHE1 might be a novel agent for the treatment of IBD without immunogenicity concerns.