DISTRIBUTION OF ACTIVATED COMPLEMENT, C3B, AND ITS DEGRADED FRAGMENTS, IC3B C3DG, IN THE COLONIC MUCOSA OF ULCERATIVE-COLITIS (UC)/

The third component of complement (C3) is central to both the classica l and alternative pathways in complement activation. In this study, in volvement of C3 activation in the mucosal injury of UC was investigate d. We examined the distribution of activated (C3b) and degraded fragme nts (iC3b/C3dg) of C3, terminal complement complex (TCC), and compleme nt regulatory proteins in normal and diseased colonic mucosa including UC and other types of colitis using immunohistochemical techniques at the level of light and electron microscopy. While C3b and iC3b/C3dg s taining was negligible in the normal mucosa, iC3b/C3dg and, to a lesse r extent, C3b were deposited in UC mucosa along the epithelial basemen t membrane. The deposition was enhanced in relation to the severity of mucosal inflammation (C3b, P < 0.05; iC3b/C3dg, P < 0.01). Epithelial deposition of TCC was not observed in most UC mucosa. Immunoelectron microscopy showed that C3b and iC3b/C3dg were distributed mainly along the epithelial basement membrane and the underlying connective tissue in a granular, studded manner, and weakly present along the basolater al surface of epithelial cells. These C3 fragments were also deposited in inflammatory control mucosa such as ischaemic and infectious colit is. Our findings suggest that deposition of the C3 fragments occurs in inflamed colonic mucosa of diverse etiologies, including UC, but to d efine a role of the deposition in the development of mucosal injury in UC awaits direct study.