Evidence map›Paper›PMID 7512985›Full record

ArticleThe Journal of clinical investigation1994

Bacterial lipopolysaccharide primes human neutrophils for enhanced release of arachidonic acid and causes phosphorylation of an 85-kD cytosolic phospholipase A2.

M E Doerfler, J Weiss, J D Clark, P Elsbach

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.7field-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

24 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
  3. Multiple Phenotypic Changes Define Neutrophil Priming.Frontiers in cellular and infection microbiology · 2017
    Review
  4. LEUKOCYTE LIPID BODIES - STRUCTURE AND FUNCTION AS "EICOSASOMES".Transactions of the American Clinical and Climatological Association · 2016
    Article
  5. Article
  6. Regulation of arachidonate remodeling enzymes impacts eosinophil survival during allergic asthma.American journal of respiratory cell and molecular biology · 2009
    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

4 authors at 1 institution in 1 country.

M E DoerflerDepartment of Medicine, New York University School of Medicine, New York 10016.
J Weiss
J D Clark
P Elsbach
New York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Production of leukotriene B4 (LTB4) by human neutrophils (PMN) in response to different stimuli is increased after pretreatment with lipopolysaccharides (LPS). We have analyzed the steps in arachidonic acid (AA) metabolism affected by LPS by examining release of AA and its metabolites from [3H]AA prelabeled PMN. Pretreatment of PMN for 60 min with up to 1 microgram/ml of LPS alone had no effect, but release of [3H]AA was stimulated up to fivefold during subsequent stimulation with a second agent. In the absence of LPS-binding protein (LBP), priming was maximal after pretreatment of PMN with 10 ng of LPS/ml for 60 min; in the presence of LBP maximal priming occurred within 45 min at 0.1 ng of LPS/ml and within 15 min at 100 ng of LPS/ml. Treatment of PMN with 10 ng of LPS/ml also increased uptake of opsonized zymosan by up to 60%. Phospholipids are the source of released [3H]AA. No release was observed from [14C]oleic acid (OA)-labeled PMN suggesting that phospholipolysis may be specific for [3H]AA-labeled phospholipid pools. Cytosol from PMN primed with LPS contains two to three times the phospholipase A2 (PLA2) activity of control PMN, against 1-palmitoyl-[2-14C]arachidonoyl-phosphatidylcholine. This activity is Ca2+ dependent and dithiothreitol resistant. LPS priming is accompanied by reduced migration during SDS-PAGE of an 85-kD protein, identified as a cytosolic PLA2. The extent and kinetics of this effect of LPS on cPLA2 parallel the priming of [3H]AA release, both depending on LPS concentration either with or without LBP. These findings suggest that priming by LPS of AA metabolism by PMN includes phosphorylation of an AA-phospholipid-selective cytosolic PLA2 that is dissociated from activation until a second stimulus is applied.

Indexed as

Acute-Phase ProteinsMembrane GlycoproteinsAlkaloidsAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticArachidonic AcidCarrier ProteinsCHO CellsCricetinaeCricetulusCytosolHumansLeukotriene B4Lipopolysaccharide-Binding ProteinLipopolysaccharide ReceptorsAcute-Phase ProteinsAlkaloidsAntigens, CDAntigens, Differentiation, MyelomonocyticArachidonic AcidCarrier ProteinsLeukotriene B4Lipopolysaccharide-Binding ProteinLipopolysaccharide ReceptorsLipopolysaccharidesMembrane GlycoproteinsPhospholipases APhospholipases A2PhospholipidsStaurosporineTetradecanoylphorbol AcetateZymosan

Identifiers

PMID7512985
PMCPMC294185
OpenAlexW2051853311

What OpenQuestion holds

Textmetadata
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.