Evidence map›Paper›PMID 26792210›Full record

ArticleThe Journal of allergy and clinical immunology2016

Activated prostaglandin D2 receptors on macrophages enhance neutrophil recruitment into the lung.

Katharina Jandl, Elvira Stacher, Zoltán Bálint, Eva Maria Sturm, Jovana Maric, Miriam Peinhaupt, Petra Luschnig, Ida Aringer, Alexander Fauland, Viktoria Konya and 7 more

Abstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 79 citations in OpenAlex.

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  16. CRTH2 in Pulmonary Fibrosis: Friend or Foe?American journal of respiratory cell and molecular biology · 2022
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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

17 authors at 3 institutions in 2 countries.

Katharina JandlInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Elvira StacherInstitute of Pathology, Medical University of Graz, Graz, Austria.
Zoltán BálintLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Eva Maria SturmInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Jovana MaricInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Miriam PeinhauptInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Petra LuschnigInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Ida AringerInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria; Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Alexander FaulandDivision of Physiological Chemistry II, Department of Medical Biochemistry and Biophysics, Stockholm, Sweden.
Viktoria KonyaInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria; Center for Infectious Medicine, Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden.
Sven-Erik DahlenInstitute of Environmental Medicine, Experimental Asthma and Allergy Research Unit, Karolinska Institutet, Stockholm, Sweden.
Craig E WheelockDivision of Physiological Chemistry II, Department of Medical Biochemistry and Biophysics, Stockholm, Sweden.
Dagmar KratkyInstitute of Molecular Biology and Biochemistry, Medical University of Graz, Graz, Austria.
Andrea OlschewskiLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.
Gunther MarscheInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Rufina SchuligoiInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria.
Akos HeinemannInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Graz, Austria. Electronic address: akos.heinemann@medunigraz.at.
Medical University of Graz · ATLudwig Boltzmann Institute for Lung Vascular Research · ATKarolinska Institutet · SE

Funding

Austrian Science Fund FWF P 22521Austrian Science Fund FWF P 25531Austrian Science Fund FWF P 26185Austrian Science Fund FWF P 27070Austrian Science Fund FWF W 1241
6 · The paper itself

Abstract

backgroundProstaglandin (PG) D2 is an early-phase mediator in inflammation, but its action and the roles of the 2 D-type prostanoid receptors (DPs) DP1 and DP2 (also called chemoattractant receptor-homologous molecule expressed on T(H)2 cells) in regulating macrophages have not been elucidated to date.

objectiveWe investigated the role of PGD2 receptors on primary human macrophages, as well as primary murine lung macrophages, and their ability to influence neutrophil action in vitro and in vivo.

methodsIn vitro studies, including migration, Ca(2+) flux, and cytokine secretion, were conducted with primary human monocyte-derived macrophages and neutrophils and freshly isolated murine alveolar and pulmonary interstitial macrophages. In vivo pulmonary inflammation was assessed in male BALB/c mice.

resultsActivation of DP1, DP2, or both receptors on human macrophages induced strong intracellular Ca(2+) flux, cytokine release, and migration of macrophages. In a murine model of LPS-induced pulmonary inflammation, activation of each PGD2 receptor resulted in aggravated airway neutrophilia, tissue myeloperoxidase activity, cytokine contents, and decreased lung compliance. Selective depletion of alveolar macrophages abolished the PGD2-enhanced inflammatory response. Activation of PGD2 receptors on human macrophages enhanced the migratory capacity and prolonged the survival of neutrophils in vitro. In human lung tissue specimens both DP1 and DP2 receptors were located on alveolar macrophages along with hematopoietic PGD synthase, the rate-limiting enzyme of PGD2 synthesis.

conclusionFor the first time, our results show that PGD2 markedly augments disease activity through its ability to enhance the proinflammatory actions of macrophages and subsequent neutrophil activation.

Indexed as

AnimalsCalcium SignalingChemotaxis, LeukocyteCytokinesEndotoxinsGene ExpressionHumansInflammation MediatorsLungLung InjuryMacrophagesMiceNeutrophil InfiltrationNeutrophilsProstaglandin D2Receptors, ImmunologicCytokinesEndotoxinsInflammation MediatorsProstaglandin D2prostaglandin D2 receptorReceptors, ImmunologicReceptors, ProstaglandinTumor Necrosis Factor-alphaD-type prostanoid receptor 1D-type prostanoid receptor 2/chemoattractant receptor–homologous molecule expressed on T(H)2 cellshematopoietic prostaglandin D synthasemacrophagesneutrophilsprostaglandin D(2)pulmonary inflammation

Identifiers

PMID26792210
PMCPMC4954606
OpenAlexW2236209760

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.