Evidence map›Paper›PMID 25765318›Full record

ArticleScientific reports2015

Genomic analysis of LPS-stimulated myeloid cells identifies a common pro-inflammatory response but divergent IL-10 anti-inflammatory responses.

Andrew Paul Hutchins, Yoshiko Takahashi, Diego Miranda-Saavedra

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  14. STAT3 Inhibits Autocrine IFN Signaling in Type I Conventional Dendritic Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Experimental and therapeutic medicine · 2020
    Article
  20. Biology and therapeutic potential of interleukin-10.The Journal of experimental medicine · 2020
    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.

Andrew Paul Hutchins1] Key Laboratory of Regenerative Biology and Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, Guangdong 510530, China [2] World Premier International (WPI) Immunology Frontier Research Center (IFReC), Osaka University, 3-1 Yamadaoka, Suita, 565-0871 Osaka, Japan.
Yoshiko Takahashi1] World Premier International (WPI) Immunology Frontier Research Center (IFReC), Osaka University, 3-1 Yamadaoka, Suita, 565-0871 Osaka, Japan [2] Center for iPS Cell Research and Application, Kyoto University, 53 Kawahara-cho, Shogoin Yoshida, Sakyo-ku, Kyoto 606-8507, Japan.
Diego Miranda-Saavedra1] World Premier International (WPI) Immunology Frontier Research Center (IFReC), Osaka University, 3-1 Yamadaoka, Suita, 565-0871 Osaka, Japan [2] Centro de Biología Molecular Severo Ochoa, CSIC/Universidad Autónoma de Madrid, 28049 Madrid, Spain [3] IE Business School, IE University, María de Molina 31 bis, 28006 Madrid, Spain.
Osaka University · JPGuangzhou Institutes of Biomedicine and Health · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is an essential physiological response to infection and injury that must be kept within strict bounds. The IL-10/STAT3 anti-inflammatory response (AIR) is indispensable for controlling the extent of inflammation, although the complete mechanisms downstream of STAT3 have not yet been elucidated. The AIR is widely known to extend to other myeloid cells, but it has best been characterized in macrophages. Here we set out to characterize the LPS-mediated pro-inflammatory response and the AIR across a range of myeloid cells. We found that whereas the LPS-induced pro-inflammatory response is broadly similar among macrophages, dendritic cells, neutrophils, mast cells and eosinophils, the AIR is drastically different across all myeloid cell types that respond to IL-10 (all bar eosinophils). We propose a model whereby the IL-10/STAT3 AIR works by selectively inhibiting specific pathways in distinct cell types: in macrophages the AIR most likely works through the inhibition of NF-κB target genes; in DCs and mast cells through indirect IRF disruption; and in neutrophils through IRF disruption and possibly also indirect NF-κB inhibition. In summary, no conserved IL-10/STAT3 AIR effectors were identified; instead a cell type-specific model of the AIR is proposed.

Indexed as

GenomicsCluster AnalysisCytokinesGene Expression ProfilingGene Expression RegulationHumansInflammationInflammation MediatorsInterleukin-10LeukocytesLipopolysaccharidesMacrophagesMyeloid CellsOrgan SpecificitySTAT3 Transcription FactorCytokinesInflammation MediatorsInterleukin-10LipopolysaccharidesSTAT3 Transcription Factor

Identifiers

PMID25765318
PMCPMC4650320
OpenAlexW2051609779

What OpenQuestion holds

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LicenceCC BY
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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.