The role of Th17/Treg balance and Th22 cell in the pathogenesis of DSS-induced colitis in mice

T-helper (Th) cells play a critical role in inflammatory bowel disease (IBD), especially the two new types: Th17 and Th22. But whether they are protective or pathogenic in the gut is still controversial. Unlike them, regulatory T (Treg) cells have undoubtedly suppressive function and can maintain immune homeostasis. Our current aims were to examine the change of Treg/Th17 balance, Th22 proportion, and the expression of Th17-related and/or Th22-related cytokines in inflammatory bowel disease. In this study, 3% dextran sulphate sodium (DSS) was administered orally to C57BL/6 mice to induce colitis. The morbidity was evaluated by daily body weight, colon length, disease activity index, and histology score of colonic lesions. Th17, Th22, and Treg cells were measured using flow cytometry. IL-17A, IL-17F, and IL-22 were quantified using enzyme linked immunosorbent assay (ELISA) kits. DSS administration induced severe clinical manifestations, such as body weight loss, colon shortening, relatively high disease activity index, and histological damage in colitis mice. Both CD4(+)IL-17A(+)IL-22(-) cells and CD4(+)IL-22(+)IL-17A(-) cells were significantly increased, which associated with the increasing expression of IL-17A, IL-17F, and IL-22. On the contrary, CD4(+)CD25(+)Foxp3(+) cells reduced. In brief, our findings clearly show that: the drift balance of Th17/Treg is apparently in DSS-induced colitis. The increasing concentration of IL-17A, IL-17F, and IL-22, as well as the increasing Th17 and Th22 cells count, suggesting Th17 and Th22 are involved in the pathological process. Further studies are warranted to develop drugs, which are effective for colitis by targeting the Th17/Treg and Th22 pathways.