Evidence map›Paper›PMID 19941004›Full record

ArticleMedical microbiology and immunology2010

Local and remote tissue injury upon intestinal ischemia and reperfusion depends on the TLR/MyD88 signaling pathway.

Tatiana Victoni, Fernando Rodrigues Coelho, Alexandre Learth Soares, Andressa de Freitas, Thomas Secher, Rodrigo Guabiraba, François Erard, Ricardo Martins de Oliveira-Filho, B Boris Vargaftig, Gregoire Lauvaux and 4 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Medical microbiology and immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

33 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Gut Microbiota Restricts NETosis in Acute Mesenteric Ischemia-Reperfusion Injury.Arteriosclerosis, thrombosis, and vascular biology · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Intestinal Ischemia-Reperfusion: Rooting for the SOCS?Digestive diseases and sciences · 2017
    Article
  15. Article
  16. Review
  17. Murine Model of Intestinal Ischemia-reperfusion Injury.Journal of visualized experiments : JoVE · 2016
    Article
  18. Article
  19. Transduced PEP-1-heme oxygenase-1 fusion protein reduces remote organ injury induced by intestinal ischemia/reperfusion.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Tatiana VictoniDepartment of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Fernando Rodrigues Coelho
Alexandre Learth Soares
Andressa de Freitas
Thomas Secher
Rodrigo Guabiraba
François Erard
Ricardo Martins de Oliveira-Filho
B Boris Vargaftig
Gregoire Lauvaux
Mamdouh A Kamal
Bernhard Ryffel
René Moser
Wothan Tavares-de-Lima
Universidade de São Paulo · BRCentre National de la Recherche Scientifique · FRCentre d’Immunologie de Marseille-Luminy · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immune responses against microorganisms may be mediated by Toll-like receptors (TLRs). Intestinal ischemia-reperfusion (i-I/R) leads to the translocation of bacteria and/or bacterial products such as endotoxin, which activate TLRs leading to acute intestinal and lung injury and inflammation observed upon gut trauma. Here, we investigated the role of TLR activation by using mice deficient for the common TLR adaptor protein myeloid differentiation factor 88 (MyD88) on local and remote inflammation following intestinal ischemia. Balb/c and MyD88(-/-) mice were subjected to occlusion of the superior mesenteric artery (45 min) followed by intestinal reperfusion (4 h). Acute neutrophil recruitment into the intestinal wall and the lung was significantly diminished in MyD88(-/-) after i-I/R, which was confirmed microscopically. Diminished neutrophil recruitment was accompanied with reduced concentration of TNF-alpha and IL-1beta level. Furthermore, diminished microvascular leak and bacteremia were associated with enhanced survival of MyD88(-/-) mice. However, neither TNF-alpha nor IL-1beta neutralization prevented neutrophil recruitment into the lung but attenuated intestinal inflammation upon i-I/R. In conclusion, our data demonstrate that disruption of the TLR/MyD88 pathway in mice attenuates acute intestinal and lung injury, inflammation, and endothelial damage allowing enhanced survival.

Indexed as

AnimalsBacteremiaBacteriaBacterial ToxinsCapillary PermeabilityHistocytochemistryInterleukin-1betaIntestinal DiseasesIntestinesIschemiaLungLung DiseasesMaleMiceMice, Inbred BALB CMice, KnockoutBacterial ToxinsInterleukin-1betaMyd88 protein, mouseMyeloid Differentiation Factor 88Toll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID19941004
OpenAlexW1993426158

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.