RELATIONSHIP OF INTERLEUKIN-1 RECEPTOR ANTAGONIST TO MUCOSAL INFLAMMATION IN INFLAMMATORY BOWEL-DISEASE

被引:24
作者
HYAMS, JS
FITZGERALD, JE
WYZGA, N
MULLER, R
TREEM, WR
JUSTINICH, CJ
KREUTZER, DL
机构
[1] HARTFORD HOSP,DEPT PATHOL,HARTFORD,CT 06102
[2] UNIV CONNECTICUT,CTR HLTH,DEPT PERIODONTOL,FARMINGTON,CT
[3] UNIV CONNECTICUT,CTR HLTH,DEPT PATHOL,FARMINGTON,CT
[4] UNIV CONNECTICUT,CTR HLTH,DEPT SURG,FARMINGTON,CT
关键词
CYTOKINES; INFLAMMATORY BOWEL DISEASE; INFLAMMATION;
D O I
10.1097/00005176-199511000-00008
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Previous work has suggested that the interleukin-1 (IL-1) receptor antagonist, IL-1ra, may regulate mucosal inflammation in inflammatory bowel disease. The present study assessed the relationship of mucosal IL-1ra levels to histologic severity of inflammation and the related proinflammatory cytokines IL-1 beta and IL-6 in children with inflammatory bowel disease. Colonic biopsy specimens from 29 patients with ulcerative colitis, 27 with Crohn's disease, and 24 noninflammatory control subjects were assayed for IL-1ra, IL-1 beta, and IL-6 by enzyme-linked immunosorbent assay. Histologic activity was graded as none, mild, moderate, or severe. Mucosal IL-1 beta levels, but not IL-1ra levels, were significantly elevated in moderate/severely inflamed biopsies from patients with either ulcerative colitis (p < 0.01) or Crohn's disease (p < 0.001) compared with those with none/mild inflammation. The mucosal molar ratio of IL-1ra/IL-1 beta was significantly lower for moderate/severe inflammation compared with none/mild inflammation for patients with ulcerative colitis (p < 0.05) and Crohn's disease (p < 0.01). The mucosal IL-1ra/IL-1 beta ratio was similar in controls to none/mild inflamed biopsies from subjects with either ulcerative colitis or Crohn's disease. Our observations suggest that increasing mucosal inflammation in inflammatory bowel disease in children is associated with a decrease in the ''normal'' effective IL-1ra/IL-1 beta ratio in which IL-1ra predominates. The importance of this abnormality to the pathogenesis of inflammatory bowel disease awaits further study.
引用
收藏
页码:419 / 425
页数:7
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