Estimation of mucosal inflammatory mediators in rat DSS-induced colitis - Possible role of PGE(2) in protection against mucosal damage

In order to investigate the mucosal injury mechanism in UC, we made dextran sulfate sodium (DSS)-induced colitis in rat and examined pathological find ings, MPO activity, PGE(2) level, and local mRNA expression and secretion o f IL-1 beta, TNF-alpha, GRO/CINC-1 and IL-10 in DSS colitis mucosa, Moreove r, we estimated the correlation between the severity of mucosal damage and changes of these local inflammatory mediators' values. Neutrophil infiltrat ion was marked and MPO activity was locally increased in proportion to the severity of mucosal damage. The mRNA expression and secretion of IL-1 beta, GRO/CINC-1 and IL-10 were increased. Especially, the secretions of IL-1 be ta and GRO/CINC-1 were increased in proportion to the severity of mucosal d amage. However, those of TNF-alpha were not increased in the colitis mucosa . An abnormal macrophage function and the presence of macrophage subtypes p roducing different cytokines would be predicted from our TNF-alpha data. Th e lesion was less severe in the colonic mucosa with higher levels of endoge nous PGE(2), while it was more severe in the colonic mucosa with lower leve ls of endogenous PGE(2), implicating this compound as an inhibitory factor against the development of inflammation in the affected mucosa. Our results suggest that PGE(2) mig ht have therapeutic applicability to UC. Copyright (C) 2001 S. Karger AG, Basel.