Elevated fibrinogen-like protein 2 in TNBS-induced colitis mice: Association with Th17 and regulatory T cells

The etiology and pathogenesis of inflammatory bowel disease (IBD) is complex and remains to be completely elucidated. Numerous cytokines are associated with the initiation and development of IBD. Fibrinogen-like protein 2 (FGL2), an immunosuppressive cytokine expressed by regulatory cluster of differentiation (CD)4(+) T (Treg) cells, has been identified to be important for immunomodulatory activity in the inflammatory state. Therefore, the present study investigated the expression of FGL2 and interleukin (IL) -17 in trinitro-benzene-sulfonic acid (TNBS) -induced colitis mice to identify the function of FGL2, based on the effector CD4(+) T helper (Th) 17/Treg balance, in IBD. Compared with control mice, TNBS-induced mice exhibited marked alterations in clinical manifestation, including macroscopic and histopathological damage. Intestinal and peripheral expression of FGL2 was upregulated in TNBS-induced mice, while the level of FGL2 in the spleen was decreased. Expression of IL-17 in the plasma, colon and spleen was increased in TNBS-induced mice. The percentage of Treg cells was markedly decreased, although Th17 cells were increased following TNBS induction. The results of the present study indicated that, in the colitis model, FGL2 was associated with the immunopathogenesis of IBD.