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Updated: Aug 17, 2026

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease
Published on: March 1, 2022
Differential role of tumor necrosis factor receptors in TNBS colitis
Dawn R Ebach1, Rodney Newberry, William F Stenson
1Division of Pediatric Gastroenterology and Nutrition, Department of Pediatrics, Washington University, St. Louis, Missouri, USA.
Background:
Tumor necrosis factor alpha (TNFalpha) 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, TNFalpha levels were increased in these mice.
Conclusions:
TNFalpha signaling through TNFR1 is protective in the trinitrobenzene sulfonic acid mouse model of inflammatory bowel disease.
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