MCP-1 Polymorphism in Behcet's disease in Korea
To compare the G vs. A variation at the MCP-1 promoter -2518 position among normal Koreans and Behcet patients, and to investigate possible association of this polymorphism with disease pathogenesis. The allele type of -2518 polymorphism was determined by restriction fragment length polymorphism of...
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Published in | Autoimmunity (Chur, Switzerland) Vol. 37; no. 1; pp. 77 - 80 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
01.02.2004
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Subjects | |
Online Access | Get full text |
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Summary: | To compare the G vs. A variation at the MCP-1 promoter -2518 position among normal Koreans and Behcet patients, and to investigate possible association of this polymorphism with disease pathogenesis. The allele type of -2518 polymorphism was determined by restriction fragment length polymorphism of Pvu II. The level of MCP-1 in serum and culture supernatent was measured by sandwich ELISA. The average serum level of MCP-1 in Behcet patients was 2.37 times higher than in normal controls. The serum MCP-1 concentration was higher in G-allele carriers than in AA homozygotes, and symptoms accompanying graver cases of Behcet's disease, such as gastrointestinal inflammation and uveitis, were more frequent in patients with the G-allele. However, the frequency of G-allele in patient group was not higher than that in healthy Koreans, probably due to the dominance of G-allele in general Korean population. When stimulated in vitro with IL-1 beta and LPS, the mononuclear cells from patients carrying the G-allele showed a steeper increase in MCP-1 production than the boost observed in AA homozygotes. Although the allele frequency of MCP-1 promoter -2518 polymorphism is not likely to be the reason for the elevated serum MCP-1 level in Korean patients with Behcet's disease, it is possible that proinflammatory factors induced in patients' serum cause stronger activation of MCP-1 expression from the G-type promoter, as well as increased incidence of uveitis and gastric ulcer, among carriers of the G-allele. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 content type line 23 ObjectType-Feature-1 |
ISSN: | 0891-6934 |