TY - JOUR
T1 - The role of the tumor necrosis factor receptor in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice
AU - Nakai, Minoru
AU - Sudo, Kaori
AU - Yamada, Yasuhiro
AU - Kojima, Yasushi
AU - Kato, Tomohiro
AU - Saito, Kuniaki
AU - Moriwaki, Hisataka
AU - Seishima, Mitsuru
N1 - Funding Information:
This work was supported by Grant-in-Aid for Scientific Research from the Ministry for Education, Culture, Sports, Science and Technology of Japan.
PY - 2005/9
Y1 - 2005/9
N2 - 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-α mRNA expression in the colon was significantly higher in all TNBS-administered groups than in controls. And NF-κ 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-κ 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.
AB - 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-α mRNA expression in the colon was significantly higher in all TNBS-administered groups than in controls. And NF-κ 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-κ 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.
KW - Apoptosis
KW - Inflammatory bowel disease
KW - NF-κ B
KW - TNF receptor
KW - TUNEL
KW - Tumor necrosis factor (TNF)
UR - https://www.scopus.com/pages/publications/23944465997
UR - https://www.scopus.com/pages/publications/23944465997#tab=citedBy
U2 - 10.1007/s10620-005-2913-1
DO - 10.1007/s10620-005-2913-1
M3 - Article
C2 - 16133967
AN - SCOPUS:23944465997
SN - 0163-2116
VL - 50
SP - 1669
EP - 1676
JO - Digestive Diseases and Sciences
JF - Digestive Diseases and Sciences
IS - 9
ER -