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TUMOR-NECROSIS-FACTOR-ALPHA INTERLEUKIN-1-BETA, AND INTERLEUKIN-6 EXPRESSION IN INFLAMMATORY BOWEL-DISEASE
被引:318
|作者:
STEVENS, C
WALZ, G
SINGARAM, C
LIPMAN, ML
ZANKER, B
MUGGIA, A
ANTONIOLI, D
PEPPERCORN, MA
STROM, TB
机构:
[1] BETH ISRAEL HOSP, DEPT MED, CTR INFLAMMATORY BOWEL DIS, BOSTON, MA 02215 USA
[2] HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA
关键词:
CROHNS DISEASE;
ULCERATIVE COLITIS;
POLYMERASE CHAIN REACTION;
INTERLEUKIN-6;
INTERLEUKIN-1;
TUMOR NECROSIS FACTOR;
D O I:
10.1007/BF01300378
中图分类号:
R57 [消化系及腹部疾病];
学科分类号:
摘要:
The etiology of ulcerative colitis (UC) and Crohn's disease (CD) remains enigmatic. Infiltrating intestinal macrophages are capable of producing the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1-beta (IL-1-beta), and interleukin-6 (IL-6). We investigated the presence of IL-6, TNF-alpha and IL-1-beta mRNA transcripts in inflammatory bowel disease (IBD), normal, and other inflammatory intestinal specimens utilizing the polymerase chain reaction (PCR). TNF-alpha mRNA levels did not vary between inflammatory bowel disease and control specimens. IL-1-beta mRNA levels were highest in active UC and noninflammatory bowel disease inflammatory specimens while IL-6 mRNA levels were highest in active IBD specimens. Infiltrating T cells, macrophages, and B cells were identified as sources of IL-6 protein in inflammatory bowel disease specimens by immunofluorescent staining. IL-6 transcripts were elevated only in active inflammatory bowel disease specimens, suggesting that IL-6-mediated immune processes are ongoing in the inflammatory mucosal environment of CD and UC.
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页码:818 / 826
页数:9
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