Differential role of tumor necrosis factor receptors in TNBS colitis

• Published in: Inflammatory bowel diseases 2005-06, Vol.11 (6), p.533-540
• Main Authors: Ebach, Dawn R, Newberry, Rodney, Stenson, William F
• Format: Article
• Language: English
• Subjects: Animals; Colitis - physiopathology; Colitis - veterinary; Disease Models, Animal; Hypothermia - etiology; inflammatory bowel disease; Mice; Mice, Inbred C57BL; Mortality; Receptors, Tumor Necrosis Factor - physiology; trinitrobenzene sulfonic acid; Trinitrobenzenesulfonic Acid - administration & dosage; Trinitrobenzenesulfonic Acid - toxicity; tumor necrosis factor receptors; tumor necrosis factor α; Tumor Necrosis Factor-alpha - analysis; Weight Loss
• ISSN: 1078-0998; 1536-4844
• DOI: 10.1097/01.MIB.0000163698.34592.30

Background: Tumor necrosis factor α (TNFα) plays a central role in the pathology of T helper 1‐mediated colitis such as Crohn's disease; however, the role of its 2 receptors in mediating pathology has not been fully explored. Methods: Trinitrobenzene sulfonic acid colitis was used to induce colitis in mice lacking each of the TNF receptors (TNFRs) and in wild‐type mice. TNFR1−/− mice lost more weight, became hypothermic, and had increased mortality compared with wild‐type C57Bl/6 mice. TNFR2−/− mice, however, lost less weight, had normal temperatures, and had improved survival. Results: Despite the improved clinical outcomes in TNFR2−/− mice, TNFα levels were increased in these mice. Conclusions: TNFα signaling through TNFR1 is protective in the trinitrobenzene sulfonic acid mouse model of inflammatory bowel disease.