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The role of the tumor necrosis factor receptor in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice.

Abstract
We investigated the effect of TNBS administration using TNF-receptor knockout mice to elucidate the role of TNF receptors in chronic inflammation of the colon. Histologically, inflammatory cell scores showed no significant differences among TNBS-administered groups, while tissue damage scores were significantly lower in TNFR-1KO and TNFR-1,2KO than in WT. The apoptotic indexes of lamina propria mononuclear cells (LPMC) of all TNBS-administered groups were significantly lower than that of controls. TNF-alpha mRNA expression in the colon was significantly higher in all TNBS-administered groups than in controls. And NF-kappa B activities were enhanced in WT and TNFR-2KO compared with controls. Our data indicate that the TNF/TNFR-1 signaling system mediates mucosal damage through the enhancement of NF-kappa B activity and that continuous infiltration of TNF-producing cells, probably a key pathogeneses of colitis, may be closely associated with defective apoptosis of LPMC, which is possibly independent of the TNF/TNFR signaling system in TNBS-induced colitis.
AuthorsMinoru Nakai, Kaori Sudo, Yasuhiro Yamada, Yasushi Kojima, Tomohiro Kato, Kuniaki Saito, Hisataka Moriwaki, Mitsuru Seishima
JournalDigestive diseases and sciences (Dig Dis Sci) Vol. 50 Issue 9 Pg. 1669-76 (Sep 2005) ISSN: 0163-2116 [Print] United States
PMID16133967 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • NF-kappa B
  • Receptors, Tumor Necrosis Factor, Type I
  • Tumor Necrosis Factor-alpha
  • Trinitrobenzenesulfonic Acid
Topics
  • Animals
  • Apoptosis
  • Colitis (chemically induced, immunology, veterinary)
  • Female
  • Inflammation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • NF-kappa B (physiology)
  • Receptors, Tumor Necrosis Factor, Type I (genetics, physiology)
  • Signal Transduction
  • Trinitrobenzenesulfonic Acid (pharmacology, toxicity)
  • Tumor Necrosis Factor-alpha (physiology)

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