Evidence map›Paper›PMID 25463476›Full record

ArticleBiochimica et biophysica acta2015

Neutrophil effector responses are suppressed by secretory phospholipase A2 modified HDL.

Sanja Curcic, Michael Holzer, Robert Frei, Lisa Pasterk, Rudolf Schicho, Akos Heinemann, Gunther Marsche

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 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
1.1field-weighted citation impact, top 24% 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, 59 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Sanja CurcicInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Austria.
Michael HolzerInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Austria.
Robert FreiInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Austria.
Lisa PasterkInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Austria.
Rudolf SchichoInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Austria.
Akos HeinemannInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Austria.
Gunther MarscheInstitute of Experimental and Clinical Pharmacology, Medical University of Graz, Austria. Electronic address: gunther.marsche@medunigraz.at.
Medical University of Graz · AT

Funding

Austrian Science Fund FWF P 22976Austrian Science Fund FWF P 25633
6 · The paper itself

Abstract

Secretory phospholipase A2 (sPLA2) generates bioactive lysophospholipids implicated in acute and chronic inflammation, but the pathophysiologic role of sPLA2 is poorly understood. Given that high-density lipoprotein (HDL) is the major substrate for sPLA2 in plasma, we investigated the effects of sPLA2-mediated modification of HDL (sPLA2-HDL) on neutrophil function, an essential arm of the innate immune response and atherosclerosis. Treatment of neutrophils with sPLA2-HDL rapidly prevented agonist-induced neutrophil activation, including shape change, neutrophil extracellular trap formation, CD11b activation, adhesion under flow and migration of neutrophils. The cholesterol-mobilizing activity of sPLA2-HDL was markedly increased when compared to native HDL, promoting a significant reduction of cholesterol-rich signaling microdomains integral to cellular signaling pathways. Moreover, sPLA2-HDL effectively suppressed agonist-induced rise in intracellular Ca²⁺ levels. Native HDL showed no significant effects and removing lysophospholipids from sPLA2-HDL abolished all anti-inflammatory activities. Overall, our studies suggest that the increased cholesterol-mobilizing activity of sPLA2-HDL and suppression of rise in intracellular Ca²⁺ levels are likely mechanism that counteracts agonist-induced activation of neutrophils. These counterintuitive findings imply that neutrophil trafficking and effector responses are altered by sPLA2-HDL during inflammatory conditions.

Indexed as

Neutrophil ActivationSignal TransductionCalciumCalcium SignalingCD11b AntigenCell AdhesionCells, CulturedCell ShapeChemotaxis, LeukocyteCholesterol, HDLExtracellular TrapsHumansImmunity, InnateImmunologic FactorsLysophosphatidylcholinesNeutrophilsCalciumCD11b AntigenCholesterol, HDLImmunologic FactorsITGAM protein, humanLysophosphatidylcholinesPhospholipases A2, SecretoryHDLLysophospholipidNeutrophilSecretory phospholipase A(2)

Identifiers

PMID25463476
PMCPMC4789498
OpenAlexW2044487577

What OpenQuestion holds

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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.