Evidence map›Paper›PMID 20004742›Full record

ArticleInternational immunopharmacology2010

Auto/paracrine control of inflammatory cytokines by acetylcholine in macrophage-like U937 cells through nicotinic receptors.

Alexander I Chernyavsky, Juan Arredondo, Maryna Skok, Sergei A Grando

Erratum issuedAbstract read
In one paragraph

Article in International immunopharmacology, 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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

34 citing papers in PubMed, 54 citations in OpenAlex.

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  6. Cholinergic Polarization of Human Macrophages.International journal of molecular sciences · 2023
    Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Alexander I ChernyavskyInstitute for Immunology, University of California, Irvine, CA 92697, USA.
Juan Arredondo
Maryna Skok
Sergei A Grando
University of California, Irvine · USPalladin Institute of Biochemistry · UA

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Christine Hui · 1994 to 2026
$57.9M
Epithelial Acetylcholine Oral Biology and PathologyR01DE014173 · NIDCR · UNIVERSITY OF CALIFORNIA-IRVINE · PI GRANDO, SERGEI A · 2002 to 2012
$3.1M
Regulation of Keratinocyte Migration by AcetylcholineR01GM062136 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GRANDO, SERGEI A · 2002 to 2010
$1.9M
Nicotinic receptor-mediated action of tobacco nitrosamines on respiratory cellsR21ES014384 · NIEHS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GRANDO, SERGEI A · 2006 to 2007
$413k
NCI NIH HHS P30 CA062203NIDCR NIH HHS DE14173NIDCR NIH HHS R01 DE014173NIEHS NIH HHS ES014384NIEHS NIH HHS R21 ES014384NIGMS NIH HHS GM62136NIGMS NIH HHS R01 GM062136
6 · The paper itself

Abstract

Although acetylcholine (ACh) is well known for its neurotransmitter function, recent studies have indicated that it also functions as an immune cytokine that prevents macrophage activation through a 'cholinergic (nicotinic) anti-inflammatory pathway'. In this study, we used the macrophage-like U937 cells to elucidate the mechanisms of the physiologic control of cytokine production by auto/paracrine ACh through the nicotinic class of ACh receptors (nAChRs) expressed in these cells. Stimulation of cells with lipopolysaccharide up-regulated expression of alpha1, alpha4, alpha5, alpha7, alpha10, beta1 and beta3 subunits, down-regulated alpha6 and beta2 subunits, and did not alter the relative quantity of alpha9 and beta4 mRNAs. Distinct nAChR subtypes showed differential regulation of the production of pro- and anti-inflammatory cytokines. While inhibition of the expression of the TNF-alpha gene was mediated predominantly by the alpha-bungarotoxin sensitive nAChRs, that of the IL-6 and IL-18 genes-by the mecamylamine-sensitive nAChRs. Both the Mec- and alphaBtx-sensitive nAChRs regulated expression of the IL-1beta gene equally efficiently. Upregulation of IL-10 production by auto/paracrine ACh was mediated predominantly through alpha7 nAChR. These findings offer a new insight on how nicotinic agonists control inflammation, thus laying a groundwork for the development of novel immunomodulatory therapies based on the nAChR subtype selectivity of nicotinic agonists.

Indexed as

Acetylcholinealpha7 Nicotinic Acetylcholine ReceptorAutocrine CommunicationBlotting, WesternCytokinesHumansImmunologic FactorsIndicators and ReagentsInflammationInterleukin-10LipopolysaccharidesMacrophagesNicotinic AgonistsParacrine CommunicationReceptors, NicotinicReverse Transcriptase Polymerase Chain ReactionAcetylcholinealpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, humanCytokinesImmunologic FactorsIndicators and ReagentsInterleukin-10LipopolysaccharidesNicotinic AgonistsReceptors, Nicotinic

Identifiers

PMID20004742
PMCPMC2829366
OpenAlexW2031922040

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.