title: Inflammation enhances resection-induced intestinal adaptive growth in IL-10 null mice.
abstract: BACKGROUND
  Surgical resection of the ileum, cecum, and proximal right colon (ICR) is common in the management of Crohn's disease, yet little is known about the effect of active inflammation on the adaptive response following intestinal loss. We recently developed a surgical model of ICR in germ-free (GF) IL-10 null mice that develop small intestinal inflammation only when mice undergo conventionalization with normal fecal microflora (CONV) before surgical intervention. In this study, we examined the effects of postsurgical small bowel inflammation on adaptive growth after ICR.
  
  
  METHODS
  GF 129SvEv IL-10 null mice, 8-10 wk old, were allocated to GF or CONV groups. Nonoperated GF and CONV mice provided baseline controls. Two wk later, GF and CONV mice were further allocated to ICR or sham operation. Small intestine and colon were harvested 7 d after surgery for histological analysis.
  
  
  RESULTS
  All mice within the gnotobiotic facility maintained GF status and did not develop small intestinal or colonic inflammation. CONV resulted in colitis in all groups, whereas small intestinal inflammation was only observed following ICR. Resection-induced small intestinal inflammation in CONV mice was associated with increases in proliferation, crypt depth, and villus height compared with GF mice after ICR. Resection-induced increases in crypt fission only occurred in CONV mice.
  
  
  CONCLUSIONS
  ICR-dependent small intestinal inflammation in CONV IL-10 null mice dramatically enhances early adaptive growth of the small intestine. Additional studies utilizing our model may provide clinical insight leading to optimal therapies in managing IBD patients after surgical resection.
authors.affiliation: Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
authors.forename: Karen E
authors.initials: KE
authors.lastname: Speck
authors.forename: Aaron P
authors.initials: AP
authors.lastname: Garrison
authors.forename: Rachael J
authors.initials: RJ
authors.lastname: Rigby
authors.forename: Doug C
authors.initials: DC
authors.lastname: von Allmen
authors.forename: P Kay
authors.initials: PK
authors.lastname: Lund
authors.forename: Michael A
authors.initials: MA
authors.lastname: Helmrath
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology; D000818:Animals; D003106:Colon / Q000254:growth & development* / Q000382:microbiology / Q000601:surgery*; D005856:Germ-Free Life; D007249:Inflammation / Q000503:physiopathology*; D016753:Interleukin-10 / Q000235:genetics* / Q000502:physiology; D007421:Intestine, Small / Q000254:growth & development* / Q000382:microbiology / Q000601:surgery*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D023421:Models, Animal
chemical_list: D016753:Interleukin-10