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A new animal model of postsurgical bowel inflammation and fibrosis: the effect of commensal microflora

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A new animal model of postsurgical bowel inflammation and fibrosis: the effect of commensal microflora. / Rigby, R. J.; Hunt, M. R.; Scull, B. P. et al.
In: Gut, Vol. 58, No. 8, 08.2009, p. 1104-1112.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Rigby, RJ, Hunt, MR, Scull, BP, Simmons, JG, Speck, KE, Helmrath, MA & Lund, PK 2009, 'A new animal model of postsurgical bowel inflammation and fibrosis: the effect of commensal microflora', Gut, vol. 58, no. 8, pp. 1104-1112. https://doi.org/10.1136/gut.2008.157636

APA

Rigby, R. J., Hunt, M. R., Scull, B. P., Simmons, J. G., Speck, K. E., Helmrath, M. A., & Lund, P. K. (2009). A new animal model of postsurgical bowel inflammation and fibrosis: the effect of commensal microflora. Gut, 58(8), 1104-1112. https://doi.org/10.1136/gut.2008.157636

Vancouver

Rigby RJ, Hunt MR, Scull BP, Simmons JG, Speck KE, Helmrath MA et al. A new animal model of postsurgical bowel inflammation and fibrosis: the effect of commensal microflora. Gut. 2009 Aug;58(8):1104-1112. doi: 10.1136/gut.2008.157636

Author

Rigby, R. J. ; Hunt, M. R. ; Scull, B. P. et al. / A new animal model of postsurgical bowel inflammation and fibrosis : the effect of commensal microflora. In: Gut. 2009 ; Vol. 58, No. 8. pp. 1104-1112.

Bibtex

@article{21593bc26bbb475a8b0403d75d1a3806,
title = "A new animal model of postsurgical bowel inflammation and fibrosis: the effect of commensal microflora",
abstract = "Objective: Ileocaecal resection (ICR) is common in Crohn's disease. Inflammation and fibrosis frequently recur at the site of anastomosis or in the small intestine (SI). No animal models of postsurgical inflammation and fibrosis exist. A model of ICR was developed in interleukin 10 (IL10) null and wild-type (WT) mice to test the hypothesis that ICR promotes postsurgical inflammation and fibrosis in the SI or anastomosis of genetically susceptible IL10 null, but not WT or germ-free (GF)-IL10 null mice.Methods: GF-IL10 null mice were conventionalised (CONV) and 3 weeks later randomised to ICR, transection (T) or no treatment (NoTx). Age-matched conventionally raised (CONV) WT and GF-IL10 null mice received ICR, T or NoTx. Animals were killed 28 days later. Histological scoring, real-time PCR for tumour necrosis factor a and collagen, and immunostaining for CD3(+) T cells assessed inflammation and fibrosis.Results: After ICR, CONV-IL10 null, but not CONV-WT mice, developed significant inflammation and fibrosis in the SI and inflammation in anastomosis compared with NoTx or T controls. Fibrosis occurred in the anastomosis of both CONV-IL10 null and CONV-WT mice following ICR. GF-IL10 null mice developed little or no inflammation or fibrosis in the SI or anastomosis after ICR.Conclusions: ICR in CONV-IL10 null mice provides a new animal model of postsurgical inflammation and fibrosis in the SI and anastomosis. Absence of inflammation and fibrosis in the SI of CONV-WT and GF-IL10 null mice following ICR indicates that postsurgical small bowel disease occurs only in genetically susceptible IL10 null mice and is bacteria dependent.",
keywords = "POSTOPERATIVE CROHNS-DISEASE, PLACEBO-CONTROLLED TRIAL, DOUBLE-BLIND, INTESTINAL INFLAMMATION, GROWTH-HORMONE, PROBIOTICS, RESECTION, ANTIBIOTICS, RECURRENCE, THERAPY",
author = "Rigby, {R. J.} and Hunt, {M. R.} and Scull, {B. P.} and Simmons, {J. G.} and Speck, {K. E.} and Helmrath, {M. A.} and Lund, {P. K.}",
year = "2009",
month = aug,
doi = "10.1136/gut.2008.157636",
language = "English",
volume = "58",
pages = "1104--1112",
journal = "Gut",
issn = "0017-5749",
publisher = "BMJ Publishing Group",
number = "8",

}

RIS

TY - JOUR

T1 - A new animal model of postsurgical bowel inflammation and fibrosis

T2 - the effect of commensal microflora

AU - Rigby, R. J.

AU - Hunt, M. R.

AU - Scull, B. P.

AU - Simmons, J. G.

AU - Speck, K. E.

AU - Helmrath, M. A.

AU - Lund, P. K.

PY - 2009/8

Y1 - 2009/8

N2 - Objective: Ileocaecal resection (ICR) is common in Crohn's disease. Inflammation and fibrosis frequently recur at the site of anastomosis or in the small intestine (SI). No animal models of postsurgical inflammation and fibrosis exist. A model of ICR was developed in interleukin 10 (IL10) null and wild-type (WT) mice to test the hypothesis that ICR promotes postsurgical inflammation and fibrosis in the SI or anastomosis of genetically susceptible IL10 null, but not WT or germ-free (GF)-IL10 null mice.Methods: GF-IL10 null mice were conventionalised (CONV) and 3 weeks later randomised to ICR, transection (T) or no treatment (NoTx). Age-matched conventionally raised (CONV) WT and GF-IL10 null mice received ICR, T or NoTx. Animals were killed 28 days later. Histological scoring, real-time PCR for tumour necrosis factor a and collagen, and immunostaining for CD3(+) T cells assessed inflammation and fibrosis.Results: After ICR, CONV-IL10 null, but not CONV-WT mice, developed significant inflammation and fibrosis in the SI and inflammation in anastomosis compared with NoTx or T controls. Fibrosis occurred in the anastomosis of both CONV-IL10 null and CONV-WT mice following ICR. GF-IL10 null mice developed little or no inflammation or fibrosis in the SI or anastomosis after ICR.Conclusions: ICR in CONV-IL10 null mice provides a new animal model of postsurgical inflammation and fibrosis in the SI and anastomosis. Absence of inflammation and fibrosis in the SI of CONV-WT and GF-IL10 null mice following ICR indicates that postsurgical small bowel disease occurs only in genetically susceptible IL10 null mice and is bacteria dependent.

AB - Objective: Ileocaecal resection (ICR) is common in Crohn's disease. Inflammation and fibrosis frequently recur at the site of anastomosis or in the small intestine (SI). No animal models of postsurgical inflammation and fibrosis exist. A model of ICR was developed in interleukin 10 (IL10) null and wild-type (WT) mice to test the hypothesis that ICR promotes postsurgical inflammation and fibrosis in the SI or anastomosis of genetically susceptible IL10 null, but not WT or germ-free (GF)-IL10 null mice.Methods: GF-IL10 null mice were conventionalised (CONV) and 3 weeks later randomised to ICR, transection (T) or no treatment (NoTx). Age-matched conventionally raised (CONV) WT and GF-IL10 null mice received ICR, T or NoTx. Animals were killed 28 days later. Histological scoring, real-time PCR for tumour necrosis factor a and collagen, and immunostaining for CD3(+) T cells assessed inflammation and fibrosis.Results: After ICR, CONV-IL10 null, but not CONV-WT mice, developed significant inflammation and fibrosis in the SI and inflammation in anastomosis compared with NoTx or T controls. Fibrosis occurred in the anastomosis of both CONV-IL10 null and CONV-WT mice following ICR. GF-IL10 null mice developed little or no inflammation or fibrosis in the SI or anastomosis after ICR.Conclusions: ICR in CONV-IL10 null mice provides a new animal model of postsurgical inflammation and fibrosis in the SI and anastomosis. Absence of inflammation and fibrosis in the SI of CONV-WT and GF-IL10 null mice following ICR indicates that postsurgical small bowel disease occurs only in genetically susceptible IL10 null mice and is bacteria dependent.

KW - POSTOPERATIVE CROHNS-DISEASE

KW - PLACEBO-CONTROLLED TRIAL

KW - DOUBLE-BLIND

KW - INTESTINAL INFLAMMATION

KW - GROWTH-HORMONE

KW - PROBIOTICS

KW - RESECTION

KW - ANTIBIOTICS

KW - RECURRENCE

KW - THERAPY

UR - http://www.scopus.com/inward/record.url?scp=67650239557&partnerID=8YFLogxK

U2 - 10.1136/gut.2008.157636

DO - 10.1136/gut.2008.157636

M3 - Journal article

VL - 58

SP - 1104

EP - 1112

JO - Gut

JF - Gut

SN - 0017-5749

IS - 8

ER -