Evidence map›Paper›PMID 26444420›Full record

ArticlePloS one2015

Leukotriene B4 Enhances NOD2-Dependent Innate Response against Influenza Virus Infection.

Manon Le Bel, Jean Gosselin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
0.4field-weighted citation impact, top 36% 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, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Leukotrienes in Innate Immunity: Still Underappreciated after All These Years?Journal of immunology (Baltimore, Md. : 1950) · 2023
    Review
  6. Article
  7. Article
  8. Frontiers in cellular and infection microbiology · 2022
    Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
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.

Manon Le BelLaboratory of Innate Immunology, CHU de Québec-Université Laval Research Center, Quebec, Canada.
Jean GosselinLaboratory of Innate Immunology, CHU de Québec-Université Laval Research Center, Quebec, Canada; Department of Molecular Medicine, Faculty of Medicine, Université Laval, Quebec, Canada.
Université Laval · CA

Funding

Canadian Institutes of Health Research MOP-115078Canadian Institutes of Health Research MOP-123440
6 · The paper itself

Abstract

Leukotriene B4 (LTB4), a central mediator of inflammation, is well known for its chemoattractant properties on effectors cells of the immune system. LTB4 also has the ability to control microbial infection by improving host innate defenses through the release of antimicrobial peptides and modulation of intracellular Toll-like receptors (TLRs) expression in response to agonist challenge. In this report, we provide evidences that LTB4 acts on nucleotide-binging oligomerization domain 2 (NOD2) pathway to enhance immune response against influenza A infection. Infected mice receiving LTB4 show improved survival, lung architecture and reduced lung viral loads as compared to placebo-treated animals. NOD2 and its downstream adaptor protein IPS-1 have been found to be essential for LTB4-mediated effects against IAV infection, as absence of NOD2 or IPS-1 diminished its capacity to control viral infection. Treatment of IAV-infected mice with LTB4 induces an increased activation of IPS-1-IRF3 axis leading to an enhanced production of IFNβ in lungs of infected mice. LTB4 also has the ability to act on the RICK-NF-κB axis since administration of LTB4 to mice challenged with MDP markedly increases the secretion of IL-6 and TNFα in lungs of mice. TAK1 appears to be essential to the action of LTB4 on NOD2 pathway since pretreatment of MEFs with TAK1 inhibitor prior stimulation with IAV or MDP strongly abrogated the potentiating effects of LTB4 on both IFNβ and cytokine secretion. Together, our results demonstrate that LTB4, through its ability to activate TAK1, potentiates both IPS-1 and RICK axis of the NOD2 pathway to improve host innate responses.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsImmunity, InnateInflammationInterferon-betaInterferon Regulatory Factor-3Interleukin-6Leukotriene B4LipopolysaccharidesLungMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMice, Inbred C57BLNF-kappa BNod2 Signaling Adaptor ProteinAdaptor Proteins, Signal TransducingInterferon-betaInterferon Regulatory Factor-3Interleukin-6Irf3 protein, mouseLeukotriene B4LipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMAVS protein, mouseNF-kappa BNod2 protein, mouseNod2 Signaling Adaptor Protein

Identifiers

PMID26444420
PMCPMC4596707
OpenAlexW2203291811

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.