Evidence map›Paper›PMID 21726510›Full record

ArticleGastroenterology2011

Chronic intestinal inflammation induces stress-response genes in commensal Escherichia coli.

Laura G Patwa, Ting-Jia Fan, Sandrine Tchaptchet, Yang Liu, Yves A Lussier, R Balfour Sartor, Jonathan J Hansen

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

53 citing papers in PubMed, 87 citations in OpenAlex.

  1. Trial
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  6. The Oncobiome in Gastroenteric and Genitourinary Cancers.International journal of molecular sciences · 2022
    Review
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  8. Article
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  12. Article
  13. Article
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  15. AFrontiers in microbiology · 2021
    Article
  16. Review
  17. Article
  18. Article
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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 2 institutions in 1 country.

Laura G PatwaCenter for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7032, USA.
Ting-Jia Fan
Sandrine Tchaptchet
Yang Liu
Yves A Lussier
R Balfour Sartor
Jonathan J Hansen
University of North Carolina at Chapel Hill · USUniversity of Chicago · US

Funding

Nation Center: Multi-Scale Study- Cellular Networks(RMI)U54CA121852 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CALIFANO, ANDREA · 2005 to 2015
$37.4M
PILOT AND FEASIBILITY STUDIESP30DK034987 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERT S. SANDLER · 1985 to 2026
$30.5M
GASTROENTEROLOGY RESEARCH TRAININGT32DK007737 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHEHZAD Z. SHEIKH · 1996 to 2026
$7.8M
Colitis Induced by immune responses to luminal bacteria-mouseR01DK053347 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SARTOR, RYAN B · 1998 to 2012
$4.6M
NATIONAL GNOTOBIOTIC RODENT RESOURCE CENTER: AIDSP40RR018603 · NCRR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SARTOR, RYAN B · 2004 to 2011
$4.0M
Bacterial Stress Responses to Intestinal InflammationK08DK087896 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HANSEN, JONATHAN JAMES · 2010 to 2014
$766k
NCI NIH HHS 1U54CA121852-01A1NCI NIH HHS U54 CA121852NCRR NIH HHS P40 RR018603NCRR NIH HHS P40 RR18803NIDDK NIH HHS K08 DK087896NIDDK NIH HHS P30 DK034987NIDDK NIH HHS P30 DK34987NIDDK NIH HHS R01 DK053347NIDDK NIH HHS R01 DK53347NIDDK NIH HHS T32 DK007737
6 · The paper itself

Abstract

BACKGROUND &

aimsIntestinal microbes induce homeostatic mucosal immune responses, but can also cause inappropriate immune activation in genetically susceptible hosts. Although immune responses to bacterial products have been studied extensively, little is known about how intestinal inflammation affects functions of commensal luminal microbes.

methodsMicroarrays and real-time polymerase chain reaction were used to profile transcriptional changes in luminal bacteria from wild-type and IL-10(-/-) mice monoassociated with a nonpathogenic, murine isolate of Escherichia coli (NC101, which causes colitis in gnotobiotic IL-10(-/-) mice). Colonic inflammation and innate and adaptive immune responses were measured in wild-type and IL-10(-/-) mice monoassociated with mutant NC101 that lack selected, up-regulated genes, and in IL-10(-/-) mice that were colonized with a combination of mutant and parental NC101. We measured intracellular survival of bacteria within primary macrophages from mice and resulting production of tumor necrosis factor.

resultsBacteria from IL-10(-/-) mice with colitis had significant up-regulation of the stress-response regulon, including the small heat shock proteins IbpA and IbpB that protect E coli from oxidative stress, compared to healthy, wild-type controls. In IL-10(-/-) mice, expression of ibpAB reduced histologic signs of colon inflammation, secretion of interleukin-12/23p40 in colonic explant cultures, serologic reactivity to NC101 antigens, and secretion of interferon-gamma by stimulated mesenteric lymph node cells. Infection of primary macrophages by bacteria that express ibpAB was associated with decreased intracellular survival and reduced secretion of tumor necrosis factor.

conclusionsChronic intestinal inflammation causes functional alterations in gene expression in commensal gut bacterium (E coli NC101). Further studies of these expression patterns might identify therapeutic targets for patients with inflammatory bowel diseases.

Indexed as

AnimalsCell LineChronic DiseaseColitisDisease Models, AnimalEscherichia coliEscherichia coli ProteinsGene Expression Regulation, BacterialHeat-Shock ProteinsInterleukin-10MiceMice, KnockoutStress, PhysiologicalTumor Necrosis Factor-alphaEscherichia coli ProteinsHeat-Shock ProteinsIbpA protein, E coliIbpB protein, E coliInterleukin-10Tumor Necrosis Factor-alpha

Identifiers

PMID21726510
PMCPMC3624969
OpenAlexW1970279206

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.