Evidence map›Paper›PMID 25179131›Full record

ArticleImmunology2015

Carbon monoxide down-modulates Toll-like receptor 4/MD2 expression on innate immune cells and reduces endotoxic shock susceptibility.

Sebastián A Riquelme, Susan M Bueno, Alexis M Kalergis

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Gases in Sepsis: Novel Mediators and Therapeutic Targets.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Self-regulation of the inflammatory response by peroxisome proliferator-activated receptors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  14. Carbon monoxide in lung cell physiology and disease.American journal of physiology. Cell physiology · 2018
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Attenuated heme oxygenase-1 responses predispose the elderly to pulmonary nontuberculous mycobacterial infections.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  20. 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

3 authors at 2 institutions in 2 countries.

Sebastián A RiquelmeMillennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile; INSERM, UMR 1064, Nantes, France.
Susan M Bueno
Alexis M Kalergis
Inserm · FRPontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carbon monoxide (CO) has been recently reported as the main anti-inflammatory mediator of the haem-degrading enzyme haem-oxygenase 1 (HO-1). It has been shown that either HO-1 induction or CO treatment reduces the ability of monocytes to respond to inflammatory stimuli, such as lipopolysaccharide (LPS), due to an inhibition of the signalling pathways leading to nuclear factor-κB, mitogen-activated protein kinases and interferon regulatory factor 3 activation. Hence, it has been suggested that CO impairs the stimulation of the Toll-like receptor 4 (TLR4)/myeloid differentiation factor-2 (MD2) complex located on the surface of immune cells. However, whether CO can negatively modulate the surface expression of the TLR4/MD2 complex in immune cells remains unknown. Here we report that either HO-1 induction or treatment with CO decreases the surface expression of TLR4/MD2 in dendritic cells (DC) and neutrophils. In addition, in a septic shock model of mice intraperitoneally injected with lipopolysaccharide (LPS), prophylactic treatment with CO protected animals from hypothermia, weight loss, mobility loss and death. Further, mice pre-treated with CO and challenged with LPS showed reduced recruitment of DC and neutrophils to peripheral blood, suggesting that this gas causes a systemic tolerance to endotoxin challenge. No differences in the amount of innate cells in lymphoid tissues were observed in CO-treated mice. Our results suggest that CO treatment reduces the expression of the TLR4/MD2 complex on the surface of myeloid cells, which renders them resistant to LPS priming in vitro, as well as in vivo in a model of endotoxic shock.

Indexed as

AnimalsAntimetabolitesCarbon MonoxideCell MovementDendritic CellsEnzyme ActivationHeme Oxygenase-1HypothermiaInflammationInflammation MediatorsInterferon Regulatory Factor-3LipopolysaccharidesLymphocyte Antigen 96MiceMice, Inbred C57BLMonocytesAntimetabolitesCarbon MonoxideHeme Oxygenase-1Inflammation MediatorsInterferon Regulatory Factor-3Irf3 protein, mouseLipopolysaccharidesLy96 protein, mouseLymphocyte Antigen 96NF-kappa BTlr4 protein, mouseToll-Like Receptor 4carbon monoxidehaem-oxygenase 1lipopolysaccharideseptic shockToll-like receptor 4

Identifiers

PMID25179131
PMCPMC4298426
OpenAlexW2004516886

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.