Objective: Ileo-cecal resection (ICR) is common in Crohn’s disease (CD). Inflammation and fibrosis frequently recur at the site of anastomosis or in the small intestine (SI). No animal models of post-surgical inflammation and fibrosis exist. We developed a model of ICR in IL-10 null and wild-type (WT) mice to test the hypothesis that that ICR promotes post-surgical inflammation and fibrosis in SI or anastomosis of genetically susceptible IL-10 null, but not WT or germ free (GF)-IL-10 null mice.
Design: GF-IL-10 null mice were conventionalized (CONV) and 3 weeks later randomized to ICR, transection (T) or no treatment (NoTx). Age-matched conventionally raised (CONV) WT and GF-IL-10 null mice received ICR, T or NoTx. Animals were killed 28 days later.
Main outcome measures: Histological scoring, real-time PCR for TNFα and collagen, and immunostaining for CD3+ T cells, assessed inflammation and fibrosis.
Results: After ICR, CONV-IL-10 null, but not CONV-WT mice, developed significant inflammation and fibrosis in SI and inflammation in anastomosis compared to NoTx or T controls. Fibrosis occurred in anastomosis of both CONV-IL-10 null and CONV-WT following ICR. GF-IL-10 null mice developed little or no inflammation or fibrosis in SI or anastomosis after ICR.
Conclusions: ICR in CONV-IL-10 null mice provides a new animal model of post-surgical inflammation and fibrosis in SI and anastomosis. Absence of inflammation and fibrosis in SI of CONV-WT and GF-IL-10 null following ICR indicates that post-surgical small bowel disease occurs only in genetically susceptible IL-10 null mice and is bacteria dependent.
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.