Increased expression of decay-accelerating factor (CD55) in the inflamed mucosa of patients with ulcerative colitis

Decay-accelerating factor (DAF) protects host tissue from the attack of autologous complement activation. To evaluate the participation of complement-mediated immune responses in the pathogenesis of ulcerative colitis (UC), we performed an immunohistochemical examination of DAF expression in the colonic mucosa of patients with UC. In normal colonic mucosa, DAF expression was negligible on the epithelium. However, weak expression was sporadically detected on the epithelium at inactive lesion of UC patients. In the inflamed mucosa of active UC patients, DAF expression was markedly enhanced as compared with normal mucosa. DAF was detected at the luminal surface of the mucosa (apical surface of the epithelium). This expression was stronger at the upper part of the crypt than the lower part of the crypt. Our results indicate that activity to protect host tissues from complement activation is enhanced in the inflamed mucosa of UC patients, suggesting that complement-mediated immune responses may be involved in the pathogenesis of this chronic inflammatory bowel disease of unknown etiology.