T-Bet Is Dependent on Stat-4 Inhibiting Acute Colitis but Not Stat-1 Using L4 Somatic Antigen of .

Helminths may alter the immunoinflammatory reactions of colitis. Proteins derived from have prospective therapy for colitis. The goal of this study was to interpret the protective mechanisms of L4 somatic antigen (LSA) from against an inflammatory response to the pathogenesis of DNBS-induced colitis. Colitis was actuated in mice by rectal instillation of DNBS. The mice were randomly divided into five groups containing control, DNBS alone, and three groups, with different doses of LSA (50, 100, and 200 g/mL), respectively. Mice initiated colitis by rectal administration of DNBS and after that were immunized with LSA for 14 days. Mice treated with LSA inhibited wasting disease compared with DNBS only group. of producing IFN- were reduced by LSA treatment. The level of T lymphocytes CD4IFN- cells in the LPL was significantly diminished by LSA at both 100 and 200 g/mL groups (<0.05). The mRNA expression of T-bet was significantly declined in LSA immunized mice, but not ROR-T mRNA, whereas GATA-3 expression tended to increase. The activation of STAT-4 significantly reduced LSA-treated mice but not STAT-1. It can be concluded that is required for optimal production of - in colitis.