Evidence map›Paper›PMID 17218614›Full record

ArticleAmerican journal of respiratory cell and molecular biology2007

Regulation of eosinophil adhesion by lysophosphatidylcholine via a non-store-operated Ca2+ channel.

Xiangdong Zhu, Jonathan Learoyd, Sanober Butt, Lilly Zhu, Peter V Usatyuk, Viswanathan Natarajan, Nilda M Munoz, Alan R Leff

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Lp-PLA2-derived LysoPC drives dendritic cell immunogenic activation and Th17 inflammation in severe asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

8 authors at 1 institution in 1 country.

Xiangdong ZhuSection of Pulmonary and Critical Care Medicine, Department of Medicine, MC6076, University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637, USA. xzhu@medicine.bsd.uchicago.edu
Jonathan Learoyd
Sanober Butt
Lilly Zhu
Peter V Usatyuk
Viswanathan Natarajan
Nilda M Munoz
Alan R Leff
University of Chicago · US

Funding

T CELL CO-STIMULATION IN ALLERGIC ASTHMAP50HL056399 · NHLBI · UNIVERSITY OF CHICAGO · PI WHITE, STEVEN R · 1996 to 2005
$9.1M
MECHANISMS OF AIRWAY HYPERRESPONSIVENESSR01HL046368 · NHLBI · UNIVERSITY OF CHICAGO · PI LEFF, ALAN RICHARD · 1991 to 2005
$1.7M
Mechanisms of Eosinophil AdhesionK08AI052109 · NIAID · UNIVERSITY OF CHICAGO · PI ZHU, XIANGDONG · 2002 to 2006
$429k
NHLBI NIH HHS HL-46368NHLBI NIH HHS HL-56399NIAID NIH HHS AI52109
6 · The paper itself

Abstract

We examined the mechanism by which lysophosphatidylcholine (LPC) regulates beta2-integrin-mediated adhesion of eosiniophils. Eosinophils were isolated from blood of mildly atopic volunteers by negative immunomagnetic selection. beta2-integrin-dependent adhesion of eosinophils to plated bovine serum albumin (BSA) was measured by residual eosinophil peroxidase activity. LPC caused maximal adhesion of eosinophils to plated BSA at 4 microM. Lysophosphatidylinositol, which has a similar molecular shape, mimicked the effect of LPC on eosinophil adhesion, while neither lysophosphatidylserine nor lysophosphatidylethanolamine had any effect. Phosphatidylethanolamine, a lipid that has a molecular orientation that is the inverse of LPC, blocked eosinophil adhesion caused by LPC. Unlike platelet-activating factor, a G-protein-coupled receptor agonist, LPC did not cause Ca2+-store depletion, but caused increased Ca2+ influx upon addition of Ca2+ to extracellular medium. This influx was not inhibited by U73122, a phospholipase C inhibitor, demonstrating independence from the G protein-activated phospholipase C pathway. Ca2+ influx was inhibited by either preincubation of phosphotidylethanolamine or La3+, a broad spectrum blocker of cation channels. LPC induced up-regulation of the active conformation of CD11b, which was blocked by preincubation with phosphatidylethanolamine. These data suggest that LPC causes a non-store-operated Ca2+ influx into eosinophils, which subsequently activates CD11b/CD18 to promote eosinophil adhesion.

Indexed as

Calcium ChannelsCD11b AntigenCell AdhesionEgtazic AcidEosinophilsGene Expression RegulationGTP-Binding ProteinsHumansLysophosphatidylcholinesMacrophage-1 AntigenPhosphatidylethanolaminesProtein ConformationRNA, MessengerSerum Albumin, BovineSignal TransductionSolubilityCalcium ChannelsCD11b AntigenEgtazic AcidGTP-Binding ProteinsLysophosphatidylcholinesMacrophage-1 AntigenphosphatidylethanolaminePhosphatidylethanolaminesRNA, MessengerSerum Albumin, BovineTransient Receptor Potential Channels

Identifiers

PMID17218614
PMCPMC1899330
OpenAlexW2101455397

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.