Abstract
P were examined with western blotting and a mannitol flux study, respectively. 2. Cell surface molecules of intestinal epithelia were separately blocked by their inhibitors or neutralizing antibodies and the change of the function of the effective molecule was tested to identify the epithelial sensing system for poly P. 3. Histological severity, cytokine induction in the colon, and the survival rate in DSS (3-4%) -induced acute colitis mice treated with intra-rectal administrations of poly P was examined. Furthermore, in the chronic phase of DSS- induced colitis mouse induced by DSS, the alterations of histological severity, cytokine induction and the activations of cell signal transductions by the intra-rectal administration of the poly P were examined. Results: 1. The synthesized poly P induced HSP27, phosphorylated p38 MAPK mouse intestinal epithelia, and suppressed intestinal permeability under oxidant stress. 2. These poly P functions were reduced by the inhibitor for integrin B1. 3. The daily intra-rectal administration of poly P improved the inflammation and survival in the acute colitis model. In chronic experimental colitis, poly P reduced the NF-kB activity that have become excessively activated in chronic experimental colitis and also improved the intestinal injury of the mouse colon. Conclusion: These findings suggest that poly P plays an important role in maintaining intestinal homeostasis and improving both acute and chronic inflammation through the integrin-p38 MAPK pathway, which is a novel system for mediating host-bacterial interactions.
Published Version
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