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PubMed2005

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

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.

Animals↗
PubMed1990

Intrathymic T cell repertoire after prenatal trinitrobenzene-sulfonic acid-treatment.

It is still a matter of debate, whether tolerance toward self-non-MHC antigens is due to intrathymic deletion or to regulatory processes in the periphery. To further pursue this question, responsiveness toward TNP and an anti-TNP monoclonal antibody (Sp6) carrying a recurrent idiotype was evaluated in prenatally trinitrobenzenesulfonic acid (TNBS)-treated mice. In prenatally untreated as well as in TNBS-treated mice, thymocytes proliferating in the absence of nominal antigen were double negative (L3T4-/Lyt2-), but antigen-specific thymocytes were single positive (L3T4+/Lyt2- or L3T4-/Lyt2+). TNBS-treated mice differed from controls inasmuch as in their first week of life T cells proliferating in response to TNP were found in the thymus and detected at increased frequencies in the spleen. The frequency of TNP-specific thymocytes and spleen cells declined rapidly, finally reaching in the spleen a level of 20-30% of controls. Furthermore, after antigenic stimulation, the frequency of thymocytes and spleen cells proliferating in response to TNP was found to be increased in control mice, but TNP-specific T cell were no more recovered in the thymus or the spleen of tolerized mice. The same accounted for thymic and splenic T cells proliferating in response to Sp6. They were expanded in control mice after antigenic stimulation, but were undetectable in TNBS-treated mice. Thus, T cells with specificity for an internal (Sp6) and an external (TNP) antigen, provided the latter was present during ontogeny, were detected in the thymus of control and, transiently, in the thymus of tolerized mice. But, the fate of antigen-specific thymocytes was different in prenatally untreated and TNBS-treated mice. The data are interpreted in the sense that tolerance toward non-MHC antigens may be acquired subsequently to tolerance toward self-MHC antigens and possibly after imprinting of antigen specificity.

Animals↗
PubMed2006

Galanin in the trinitrobenzene sulfonic acid rat model of experimental colitis.

Neuropeptides are molecules produced by a variety of cells that modulate several biological processes and modify the activity of cells responsible either to trigger tissue damage and to promote healing in the intestine. Galanin is a neuropeptide present in enteric nerves lining the gastrointestinal tract and involved in the secretion and contractility regulation. The aim of this study is to investigate its potential therapeutic experimental use in an immunological disorder, such as experimental trinitrobenzensulfonic acid (TNBS)-induced colitis in rats. Galanin (10, 20 and 40 microg/kg/day) was administered by intraperitoneal route 48, 24 and 1 h prior to the induction of colitis and 24 h later, and the animals were sacrificed 48 h after. The lesions were blindly scored according to macroscopic and histological scales. The inflammatory response was assessed by histological analysis and by myeloperoxidase activity (MPO) and tumour necrosis factor-alpha (TNF-alpha) production. The results indicated that Galanin prevented the morphological alteration and reduced ulcer index associated with TNBS. In addition, Galanin reduced MPO and TNF-alpha values significantly. In order to elucidate some of the mechanisms, cycloxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression was analyzed by Western blotting. COX-2 was not modified, but iNOS protein was significantly reduced accompanied by a diminished nitrite production, in a dose-dependent manner, in comparison to the TNBS group. In conclusion, Galanin treatment has a significant preventive effect in the TNBS-induced acute model of colitis with reduction of the analyzed inflammatory parameters. Moreover, the results obtained demonstrated by the first time that Galanin administration promotes an important reduction in NO-related mechanisms.

Animals↗