Evidence map›Paper›PMID 17255219›Full record

ArticleGut2007

Exacerbation of murine ileitis by Toll-like receptor 4 mediated sensing of lipopolysaccharide from commensal Escherichia coli.

M M Heimesaat, A Fischer, H-K Jahn, J Niebergall, M Freudenberg, M Blaut, O Liesenfeld, R R Schumann, U B Göbel, S Bereswill

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

111 citing papers in PubMed, 160 citations in OpenAlex.

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  14. ChronicProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Treatment with the Probiotic Product AviguardInternational journal of molecular sciences · 2021
    Article
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51 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 1 country.

M M HeimesaatInstitut für Mikrobiologie und Hygiene, Charité, Universitätsmedizin Berlin, Campus Charité Mitte, Dorotheenstr. 96,D-10117 Berlin, Germany.
A Fischer
H-K Jahn
J Niebergall
M Freudenberg
M Blaut
O Liesenfeld
R R Schumann
U B Göbel
S Bereswill
Charité - Universitätsmedizin Berlin · DEInstitute of Medical Microbiology and Hygiene · DEGerman Institute of Human Nutrition · DEMax Planck Institute of Immunobiology and Epigenetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn the course of inflammatory bowel diseases (IBD) and acute murine ileitis following peroral Toxoplasma gondii infection, commensal Escherichia coli accumulate at inflamed mucosal sites and aggravate small intestinal immunopathology.

aimTo unravel the molecular mechanisms by which commensal E coli exacerbate ileitis.

methodsIleitis was investigated in mice that lack Toll-like receptors (TLR) 2 or 4, specific for bacterial lipoproteins (LP) or lipopolysaccharide (LPS), respectively. Gnotobiotic mice, in which any cultivable gut bacteria were eradicated by antibiotic treatment, were used to study the role of LPS in ileitis.

resultsMicrobiological analyses revealed that E coli increase in the inflamed ileum. TLR4(-/-), but not TLR2(-/-), mice displayed reduced mortality and small intestinal immunopathology. Decreased interferon (IFN)-gamma and nitric oxide (NO) levels in the inflamed terminal ileum of TLR4(-/-) mice indicated that TLR4 signalling aggravates ileitis via local mediator release from immune cells. E coli strains isolated from the inflamed ileum activated cultured mouse macrophages and induced TLR4-dependent nuclear factor kappaB activation and NO production in human embryonic kidney 293 cells and in peritoneal macrophages, respectively. Most strikingly, in contrast with wild-type mice, gnotobiotic TLR4(-/-) mice were protected from induction of ileitis by treatment with purified E coli lipid A or colonisation with live E coli. Finally, prophylactic treatment with the LPS scavenger polymyxin B ameliorated T gondii-induced ileitis.

conclusionThese findings highlight the innate immune system as a key player in T gondii-induced ileal immunopathology. Treatment with LPS or TLR4 antagonists may represent a novel strategy for prophylaxis and/or therapy of small intestinal inflammation in IBD.

Indexed as

AnimalsAnti-Bacterial AgentsBacterial TranslocationCells, CulturedColony Count, MicrobialEscherichia coliGerm-Free LifeIleitisIleumLipopolysaccharidesMiceMice, Inbred C57BLPolymyxin BSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4Anti-Bacterial AgentsLipopolysaccharidesPolymyxin BTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID17255219
PMCPMC1994376
OpenAlexW2160929160

What OpenQuestion holds

Textmetadata
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.