Evidence map›Paper›PMID 19398439›Full record

ArticleGut2009

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

R J Rigby, M R Hunt, B P Scull, J G Simmons, K E Speck, M A Helmrath, P K Lund

Open access · greenAbstract read
In one paragraph

Article in Gut, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  14. Review
  15. Murine ileocolic bowel resection with primary anastomosis.Journal of visualized experiments : JoVE · 2014
    Article
  16. Article
  17. Review
  18. Article
  19. Prevention of post-operative recurrence of Crohn's disease.World journal of gastroenterology · 2014
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

R J RigbyDepartment of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27510, USA.
M R Hunt
B P Scull
J G Simmons
K E Speck
M A Helmrath
P K Lund
University of North Carolina at Chapel Hill · US

Funding

PILOT AND FEASIBILITY STUDIESP30DK034987 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Ryan B Sartor · 1985 to 2026
$30.5M
NATIONAL GNOTOBIOTIC RODENT RESOURCE CENTER: AIDSP40RR018603 · NCRR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SARTOR, RYAN B · 2004 to 2011
$4.0M
Mechanisms of Intestinal Stem Cell Expansion Following ResectionR01DK083325 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HELMRATH, MICHAEL A. · 2009 to 2013
$1.5M
Secretory lineages during intestinal adaptationK08DK067395 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HELMRATH, MICHAEL A. · 2004 to 2008
$650k
Mechanisms of intestinal failure in post-surgical inflammatory bowel diseaseR21DK080283 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI LUND, PAULINE K · 2008 to 2009
$403k
NCRR NIH HHS P40 RR018603NCRR NIH HHS P40RR018603NIDDK NIH HHS DK067395NIDDK NIH HHS DK080283NIDDK NIH HHS K08 DK067395NIDDK NIH HHS P30 DK034987NIDDK NIH HHS P30DK34987NIDDK NIH HHS R21 DK080283
6 · The paper itself

Abstract

objectiveIleocaecal 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.

methodsGF-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 alpha and collagen, and immunostaining for CD3(+) T cells assessed inflammation and fibrosis.

resultsAfter 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.

conclusionsICR 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.

Indexed as

Disease Models, AnimalAnastomosis, SurgicalAnimalsCecumCollagenCrohn DiseaseFibrosisGenetic Predisposition to DiseaseIleumInterleukin-10Intestine, SmallMiceMice, KnockoutPostoperative ComplicationsRecurrenceRNA, MessengerCollagenInterleukin-10RNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID19398439
PMCPMC2752281
OpenAlexW2106986926

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.