Evidence map›Paper›PMID 21903133›Full record

ArticleImmunology letters2011

TLR-induced activation of neutrophils promotes histamine production via a PI3 kinase dependent mechanism.

Craig Smuda, Joshua B Wechsler, Paul J Bryce

Abstract read
In one paragraph

Article in Immunology letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

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  10. Cardiomyocytes of the Heart and Pulmonary Veins: Novel Contributors to Asthma?American journal of respiratory cell and molecular biology · 2017
    Review
  11. Article
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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 1 institution in 1 country.

Craig SmudaDepartment of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Joshua B Wechsler
Paul J Bryce
Northwestern University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Regulation of T cell migration by histamineR01AI076456 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HULSE, KATHRYN ELIZABETH · 2008 to 2017
$3.9M
Epithelial BAFF and APRIL in Airway Inflammation, Immunity and DiseaseR01AI072570 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2007 to 2011
$2.3M
Histamine and Neutrophil Influx in the Pathogenesis of Acute Lung InjuryF30ES017378 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SMUDA, CRAIG ALEXANDER · 2009 to 2013
$193k
NCI NIH HHS CA060553NCI NIH HHS P30 CA060553NIAID NIH HHS R01 AI072570NIAID NIH HHS R01 AI076456NIEHS NIH HHS F30 ES017378
6 · The paper itself

Abstract

Histamine is a bioactive amine that exerts immunomodulatory functions, including many allergic symptoms. It is preformed and stored in mast cells and basophils but recent evidence suggests that other cell types produce histamine in an inducible fashion. During infection, it has been suggested that neutrophils may produce histamine. We also observed that histamine is released in a neutrophil-mediated LPS-induced model of acute lung injury. Therefore, we sought to examine whether innate signals promote histamine production by neutrophils. Bone marrow-derived neutrophils stimulated with a range of TLR agonists secreted histamine in response to LPS or R837, suggesting TLR4 or TLR7 are important. LPS-driven histamine was enhanced by coculture with GM-CSF and led to a transient release of histamine that peaked at 8h post stimulation. This was dependent upon de novo synthesis of histamine, since cells derived from histidine decarboxylase (HDC) deficient mice were unable to produce histamine but did generate reactive oxygen species upon stimulation. Using pharmacological inhibitors, we show that histamine production requires PI3 kinase, which has been shown to regulate other neutrophil functions, including activation and selective granule release. However, unlike mast cells, HDC deficiency did not alter the granule structure of neutrophils, suggesting that histamine does not participate in granule integrity in these cells. Consequently, our findings establish that neutrophils generate histamine in response to a select panel of innate immune triggers and that this might contribute to acute lung injury responses.

Indexed as

HistamineNeutrophilsAdministration, InhalationAnimalsBasophilsDisease Models, AnimalGranulocyte-Macrophage Colony-Stimulating FactorHistidine DecarboxylaseLipopolysaccharidesMast CellsMiceMice, Inbred C57BLMice, KnockoutPhosphatidylinositol 3-KinaseQuinolinesSignal Transduction1-(2-methylpropyl)-1H-imidazo(4,5-c)quinolin 4-amineGranulocyte-Macrophage Colony-Stimulating FactorHistamineHistidine DecarboxylaseLipopolysaccharidesPhosphatidylinositol 3-KinaseQuinolines

Identifiers

PMID21903133
PMCPMC3205215
OpenAlexW1979850597

What OpenQuestion holds

Textmetadata
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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.