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.
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Authors | Minoru Nakai, Kaori Sudo, Yasuhiro Yamada, Yasushi Kojima, Tomohiro Kato, Kuniaki Saito, Hisataka Moriwaki, Mitsuru Seishima |
Journal | Digestive diseases and sciences
(Dig Dis Sci)
Vol. 50
Issue 9
Pg. 1669-76
(Sep 2005)
ISSN: 0163-2116 [Print] United States |
PMID | 16133967
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- NF-kappa B
- Receptors, Tumor Necrosis Factor, Type I
- Tumor Necrosis Factor-alpha
- Trinitrobenzenesulfonic Acid
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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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