Tumor necrosis factor-α, interleukin-1β, and interleukin-6 expression in inflammatory bowel disease

C Stevens, G Walz, C Singaram, ML Lipman… - Digestive diseases and …, 1992 - Springer
C Stevens, G Walz, C Singaram, ML Lipman, B Zanker, A Muggia, D Antonioli…
Digestive diseases and sciences, 1992Springer
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-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). We
investigated the presence of IL-6, TNF-α and IL-1β mRNA transcripts in inflammatory bowel
disease (IBD), normal, and other inflammatory intestinal specimens utilizing the polymerase
chain reaction (PCR). TNF-α mRNA levels did not vary between inflammatory bowel disease …
Abstract
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-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). We investigated the presence of IL-6, TNF-α and IL-1β mRNA transcripts in inflammatory bowel disease (IBD), normal, and other inflammatory intestinal specimens utilizing the polymerase chain reaction (PCR). TNF-α mRNA levels did not vary between inflammatory bowel disease and control specimens. IL-1β 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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