Evidence map›Paper›PMID 25539820›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

TLR2 modulates antibodies required for intestinal ischemia/reperfusion-induced damage and inflammation.

Michael R Pope, Sherry D Fleming

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Review
  6. Article
  7. Review
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  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Therapeutic Potential of Annexin A1 in Ischemia Reperfusion Injury.International journal of molecular sciences · 2018
    Review
  15. Murine Model of Intestinal Ischemia-reperfusion Injury.Journal of visualized experiments : JoVE · 2016
    Article
  16. 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

2 authors at 1 institution in 1 country.

Michael R PopeDivision of Biology, Kansas State University, Manhattan, KS 66506.
Sherry D FlemingDivision of Biology, Kansas State University, Manhattan, KS 66506 sdflemin@ksu.edu.
Kansas State University · US

Funding

Mentoring CoreP20GM103418 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SUSAN J. BROWN · 2012 to 2026
$63.0M
UNDERSTANDING THE ROLE OF SMALL RNAS IN ARABIDOPSIS POLLEN DEVELOPMENTP20RR016475 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ACKLEY, BRIAN DOUGLAS · 2001 to 2011
$38.1M
Natural Antibodies and Tissue InjuryR01AI061691 · NIAID · KANSAS STATE UNIVERSITY · PI FLEMING, SHERRY · 2007 to 2011
$1.7M
Neoantigens and TLR4R21AI107005 · NIAID · KANSAS STATE UNIVERSITY · PI FLEMING, SHERRY · 2014 to 2015
$413k
NCRR NIH HHS P20 RR016475NCRR NIH HHS RR016475NIAID NIH HHS R01 AI061691NIAID NIH HHS R21 AI107005NIGMS NIH HHS P20 GM103418
6 · The paper itself

Abstract

In multiple clinical conditions, including trauma and hemorrhage, reperfusion magnifies ischemic tissue damage. Ischemia induces expression of multiple neoantigens, including lipid alterations that are recognized by the serum protein, β2-glycoprotein I (β2-GPI). During reperfusion, binding of β2-GPI by naturally occurring Abs results in an excessive inflammatory response that may lead to death. As β2-GPI is critical for intestinal ischemia/reperfusion (IR)-induced tissue damage and TLR2 is one of the proposed receptors for β2-GPI, we hypothesized that IR-induced intestinal damage and inflammation require TLR2. Using TLR2(-/-) mice, we demonstrate that TLR2 is required for IR-induced mucosal damage, as well as complement activation and proinflammatory cytokine production. In response to IR, TLR2(-/-) mice have increased serum β2-GPI compared with wild-type mice, but β2-GPI is not deposited on ischemic intestinal tissue. In addition, TLR2(-/-) mice also did not express other novel Ags, suggesting a sequential response. Unlike other TLRs, TLR2(-/-) mice lacked the appropriate Ab repertoire to induce intestinal IR tissue damage or inflammation. Together, these data suggest that, in addition to the inflammatory response, IR-induced injury requires TLR2 for naturally occurring Ab production.

Indexed as

AnimalsAntibodiesbeta 2-Glycoprotein IComplement System ProteinsCytokinesDisease Models, AnimalEicosanoidsImmunoglobulin MInflammationIntestinal MucosaIntestinesMiceMice, KnockoutReperfusion InjuryToll-Like Receptor 2Antibodiesbeta 2-Glycoprotein IComplement System ProteinsCytokinesEicosanoidsImmunoglobulin MToll-Like Receptor 2

Identifiers

PMID25539820
PMCPMC4297697
OpenAlexW1583359706

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.