Abstract | 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: 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.
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Authors | T Uesu, M Mizuno, H Inoue, J Tomoda, T Tsuji |
Journal | Laboratory investigation; a journal of technical methods and pathology
(Lab Invest)
Vol. 72
Issue 5
Pg. 587-91
(May 1995)
ISSN: 0023-6837 [Print] United States |
PMID | 7538183
(Publication Type: Journal Article)
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Chemical References |
- Antigens, CD
- CD55 Antigens
- CD59 Antigens
- Membrane Glycoproteins
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Topics |
- Adult
- Antigens, CD
(biosynthesis)
- CD55 Antigens
- CD59 Antigens
- Colitis, Ulcerative
(immunology, pathology)
- Colon
(immunology)
- Female
- Humans
- Intestinal Mucosa
(immunology)
- Male
- Membrane Glycoproteins
(biosynthesis)
- Microscopy, Immunoelectron
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