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Enhanced expression of decay accelerating factor and CD59/homologous restriction factor 20 on the colonic epithelium
1First Department of Internal Medicine, Okayama University Medical School, Japan.
Background:
The complement system is thought to be one of the factors involved in damaging the colonic mucosa in the pathogenesis of ulcerative colitis (UC). Several membrane-bound factors that regulate complement activation have been identified.
Experimental Design:
To elucidate alteration(s) of the complement regulatory proteins and to add to the understanding of the role of the complement-related immune responses in the pathogenesis of UC, we immunohistochemically examined the distribution of decay accelerating factor (DAF), CD59/homologous restriction factor 20 (HRF20), and membrane cofactor protein (MCP) in colonic mucosa with UC and compared it with that in normal and inflammatory control mucosae.
Results:
In normal colonic epithelia, the cell surface distribution of DAF and CD59/HRF20 was confined to the apical domain, whereas MCP was present on the basolateral surface. Although MCP expression in active UC was not significantly different from normal mucosa, DAF and CD59/HRF20 expression on epithelial cells of UC was markedly enhanced in relation to the severity of mucosal inflammation. In the colonic epithelia of active UC, DAF and CD59/HRF20 were not only overexpressed on the apical surface but also were distributed to the basolateral membrane. The altered cell surface distribution of these molecules was also confirmed by immunoelectron microscopy. The enhanced expression of DAF and CD59/HRF20 was not specific to UC but was observed in colonic mucosa of inflammatory controls, such as ischemic colitis.
Conclusions:
Our results indicate that altered regulation of complement activation is present in UC mucosa, but whether it may play a causal role in the immunologic disorders leading to UC remains to be elucidated.