Exposure Procedure And Interaction Of Different Antigen Play A Role In The Pathogenesis Of Inflammatory Bowel Disease

Exposure procedure and interaction of various intestinal antigen, as well as the individual susceptibility and pathogenic specificity of antigen, may be partly responsible for the loss of immune tolerance contributing to IBD. To veriiy the hypothesis, the study was conducted to observe whether the different exposure route of haptin TNBS and the interaction with Oxazolone influence induction of experimental colitis, and the relationship with Thl/Th2/Th3 balance.MethodsFor induction of colitis by different exposure procedure of haptins, SPF BALB/c mice were randomly divided into 4 groups. Group A: gavages of lOmg TNBS on days 1 and 8, then enema of 1 mg TNBS one week later. Group B: mere enema of lmg TNBS. Group C; simultaneous enema of lmg TNBS and lmg Oxazolone. Group D: enema of lmg Oxazolone, then enema of lmg TNBS one week later. All mice were sacrificed 7 days after colitis induction by the last enema of TNBS. Colitis was assessed according to clinical and histological parameters. The serum concentrations of IL-10, IL-4 and INF-Twere measured.ResultsCompared with group B or group C, mice in group A manifested significantly ameliorated inflammatory response according to clinical or histological assessment and an increase in EL-10 and a decrease in INF-rserum levels. Clinical response (symptoms and weight loss) in group D was significantly reduced, but the histological grading and serum concentrations of IL-10, IL-4 and INF--yshowed no differences among group B, group C and group D.ConclusionsThe two haptins have mutual antagonistic effect in the pathogenesis of experimental colitis. But it seems not to be related to the Thl/Th2 balance. Feeding of TNBS can induce oral tolerance and prevent colitis caused by enema. The mechanisms may involve in Thl/Th3 balance. In summary, exposure procedure and interaction (route, chronological order, frequency and dosage) of various antigen may be an important part of the environmental factors that contribute to the pathogenesis of inflammatory bowel disease.