Evidence map›Paper›PMID 25659107›Full record

Trial reportPloS one2015

The role of phosphoinositide 3-kinases in neutrophil migration in 3D collagen gels.

Kayleigh J S Martin, Michelle J Muessel, Christine E Pullar, Gary B Willars, Andrew J Wardlaw

Erratum issuedOpen access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Neutrophils actively swell to potentiate rapid migration.bioRxiv : the preprint server for biology · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Kayleigh J S MartinInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
Michelle J MuesselInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
Christine E PullarDepartment of Cell Physiology and Pharmacology, University of Leicester, Leicester, United Kingdom.
Gary B WillarsDepartment of Cell Physiology and Pharmacology, University of Leicester, Leicester, United Kingdom.
Andrew J WardlawInstitute for Lung Health, Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
University of Leicester · GB

Funding

Medical Research Council
6 · The paper itself

Abstract

The entry of neutrophils into tissue has been well characterised; however the fate of these cells once inside the tissue microenvironment is not fully understood. A variety of signal transduction pathways including those involving class I PI3 Kinases have been suggested to be involved in neutrophil migration. This study aims to determine the involvement of PI3 Kinases in chemokinetic and chemotactic neutrophil migration in response to CXCL8 and GM-CSF in a three-dimensional collagen gel, as a model of tissue. Using a three-dimensional collagen assay chemokinetic and chemotactic migration induced by CXCL8 was inhibited with the pan PI3 Kinase inhibitor wortmannin. Analysis of the specific Class I PI3 Kinase catalytic isoforms alpha, delta and gamma using the inhibitors PIK-75, PIK-294 and AS-605240 respectively indicated differential roles in CXCL8-induced neutrophil migration. PIK-294 inhibited both chemokinetic and chemotactic CXCL8-induced migration. AS-605240 markedly reduced CXCL8 induced chemokinetic migration but had no effect on CXCL8 induced chemotactic migration. In contrast PIK-75 inhibited chemotactic migration but not chemokinetic migration. At optimal concentrations of GM-CSF the inhibitors had no effect on the percentage of neutrophil migration in comparison to the control however at suboptimal concentrations wortmannin, AS-605240 and PIK-294 inhibited chemokinesis. This study suggests that PI3 Kinase is necessary for CXCL8 induced migration in a 3D tissue environment but that chemokinetic and chemotactic migration may be controlled by different isoforms with gamma shown to be important in chemokinesis and alpha important in chemotaxis. Neutrophil migration in response to suboptimal concentrations of GM-CSF is dependent on PI3 Kinase, particularly the gamma and delta catalytic isoforms.

Indexed as

Cell MovementCollagenEnzyme InhibitorsFemaleGelsGranulocyte-Macrophage Colony-Stimulating FactorHumansInterleukin-8MaleNeutrophilsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsCollagenCXCL8 protein, humanEnzyme InhibitorsGelsGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-8Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase Inhibitors

Identifiers

PMID25659107
PMCPMC4320071
OpenAlexW2075877111

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.