Aggravated mucosal and immune damage in a mouse model of ulcerative colitis with stress.

Abstract

The aim of the present study was to determine the influence of stress on the colonic mucosa and immune system and to further investigate the association between stress and development and pathogenesis of ulcerative colitis (UC). Mice were treated with 2,4,6-trinitrobenzenesulfonic acid to induce an animal model of UC, and stress was induced by water immersion and restraint. Subsequently, the disease activity index (DAI), secretory immunoglobulin A (sIgA), IgA, interleukin (IL)-6 and -8, tumor necrosis factor-α (TNF-α), complement component (C)3 and C4, and alterations in the colonic mucosa were observed. The DAI scores and the expression levels of IL-6, IL-8 and TNF-α significantly increased in the experimental UC mice compared with the control mice, while the expression levels of IgA and sIgA decreased (all P<0.01). DAI and colonic mucosa damage scores increased in the stress-treated mouse models of UC compared with the untreated mouse models of UC (P<0.05). Expression levels of IgA and sIgA decreased, while IL-6, IL-8 and TNF-α further increased in the stress-treated UC mice (P<0.05). The expression levels of C3 and C4 were not affected by stress or UC (P>0.05). These results indicated that UC may be associated with an immune disorder and that stress can aggravate colonic mucosa injury and alter the immune response. Furthermore, stress and immunity may serve roles in the pathogenesis of UC.