Evidence map›Paper›PMID 24312681›Full record

ArticlePloS one2013

Lysophosphatidylcholine triggers TLR2- and TLR4-mediated signaling pathways but counteracts LPS-induced NO synthesis in peritoneal macrophages by inhibiting NF-κB translocation and MAPK/ERK phosphorylation.

Alan Brito Carneiro, Bruna Maria Ferreira Iaciura, Lilian Lie Nohara, Carla Duque Lopes, Esteban Mauricio Cordero Veas, Vania Sammartino Mariano, Patricia Torres Bozza, Ulisses Gazos Lopes, Georgia Correa Atella, Igor Correia Almeida and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
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  14. Lipid signature in X-ALD: a comparison between phenotypes.Frontiers in molecular biosciences · 2026
    Article
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  20. Observational

26 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

11 authors at 5 institutions in 3 countries.

Alan Brito CarneiroInstituto de Bioquímica Médica, Programa de Biologia Molecular e Biotecnologia, CCS, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil ; Instituto Nacional de Ciência e Tecnologia em Entomologia Molecular- INCT-EM, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Bruna Maria Ferreira Iaciura
Lilian Lie Nohara
Carla Duque Lopes
Esteban Mauricio Cordero Veas
Vania Sammartino Mariano
Patricia Torres Bozza
Ulisses Gazos Lopes
Georgia Correa Atella
Igor Correia Almeida
Mário Alberto Cardoso Silva-Neto
The University of Texas at El Paso · USFundação Oswaldo Cruz · BRInstituto Nacional de Ciência e Tecnologia em Entomologia Molecular · BRUniversidade Federal do Rio de Janeiro · BRCzech Academy of Sciences, Institute of Biophysics · CZ

Funding

TOXICOLOGY PROJECTG12RR008124 · NCRR · UNIVERSITY OF TEXAS EL PASO · PI WALSH, ELIZABETH J · 1992 to 2011
$20.8M
TCCG12MD007592 · NIMHD · UNIVERSITY OF TEXAS EL PASO · PI KIRKEN, ROBERT A. · 2012 to 2018
$19.4M
NCRR NIH HHS 2G12RR008124-16A1NCRR NIH HHS 2G12RR008124-16A1S1NCRR NIH HHS G12 RR008124NIMHD NIH HHS 8G12MD007592NIMHD NIH HHS G12 MD007592
6 · The paper itself

Abstract

backgroundLysophosphatidylcholine (LPC) is the main phospholipid component of oxidized low-density lipoprotein (oxLDL) and is usually noted as a marker of several human diseases, such as atherosclerosis, cancer and diabetes. Some studies suggest that oxLDL modulates Toll-like receptor (TLR) signaling. However, effector molecules that are present in oxLDL particles and can trigger TLR signaling are not yet clear. LPC was previously described as an attenuator of sepsis and as an immune suppressor. In the present study, we have evaluated the role of LPC as a dual modulator of the TLR-mediated signaling pathway. METHODOLOGY/PRINCIPAL

findingsHEK 293A cells were transfected with TLR expression constructs and stimulated with LPC molecules with different fatty acid chain lengths and saturation levels. All LPC molecules activated both TLR4 and TLR2-1 signaling, as evaluated by NF-қB activation and IL-8 production. These data were confirmed by Western blot analysis of NF-қB translocation in isolated nuclei of peritoneal murine macrophages. However, LPC counteracted the TLR4 signaling induced by LPS. In this case, NF-қB translocation, nitric oxide (NO) synthesis and the expression of inducible nitric oxide synthase (iNOS) were blocked. Moreover, LPC activated the MAP Kinases p38 and JNK, but not ERK, in murine macrophages. Interestingly, LPC blocked LPS-induced ERK activation in peritoneal macrophages but not in TLR-transfected cells. CONCLUSIONS/SIGNIFICANCE: The above results indicate that LPC is a dual-activity ligand molecule. It is able to trigger a classical proinflammatory phenotype by activating TLR4- and TLR2-1-mediated signaling. However, in the presence of classical TLR ligands, LPC counteracts some of the TLR-mediated intracellular responses, ultimately inducing an anti-inflammatory phenotype; LPC may thus play a role in the regulation of cell immune responses and disease progression.

Indexed as

AnimalsDrug AntagonismEnzyme ActivationExtracellular Signal-Regulated MAP KinasesHumansLipopolysaccharidesLysophosphatidylcholinesMacrophages, PeritonealMaleMiceMitogen-Activated Protein KinasesNF-kappa BNitric OxidePhosphorylationProtein TransportSignal TransductionExtracellular Signal-Regulated MAP KinasesLipopolysaccharidesLysophosphatidylcholinesMitogen-Activated Protein KinasesNF-kappa BNitric OxideToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID24312681
PMCPMC3848743
OpenAlexW2138455845

What OpenQuestion holds

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Registered trials

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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.