Evidence map›Paper›PMID 23860188›Full record

ArticleJournal of innate immunity2014

CCR5 and FPR1 mediate neutrophil recruitment in endotoxin-induced lung injury.

Jochen Grommes, Maik Drechsler, Oliver Soehnlein

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 65 citations in OpenAlex.

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  19. CCR2 and CCR5 promote diclofenac-induced hepatotoxicity in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2019
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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

3 authors at 3 institutions in 2 countries.

Jochen GrommesEuropean Vascular Center Aachen-Maastricht, RWTH Aachen, Aachen, Germany.
Maik Drechsler
Oliver Soehnlein
Ludwig-Maximilians-Universität München · DERWTH Aachen University · DEUniversity of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recruitment of neutrophils, regarded as a key mechanism in acute lung injury (ALI), is orchestrated by cell adhesion molecules and chemokines. While the importance of cell adhesion molecules has been carefully investigated, little is known about the importance of chemokines and their receptors in the recruitment of neutrophils in models of ALI. Wild-type Ccr2(-/-), Ccr5(-/-), Fpr1(-/-) or Fpr2(-/-) mice were exposed to aerosolized lipopolysaccharide and the number of neutrophils in the lung tissue (intravascular, interstitial) and in the bronchoalveolar lavage was quantified. Lack of CCR5 or FPR1, but not CCR2 or FPR2, significantly reduced lung neutrophil infiltration in all compartments. Similarly, blockade of CCR5 or FPR1 with specific antagonists reduced counts of alveolar, interstitial and intravascular neutrophils. Such treatments also inhibited lung edema formation and histological lung tissue alterations, thus underscoring the protective role of CCR5 and FPR1 neutralizing strategies in ALI.

Indexed as

Acute Lung InjuryAnimalsCCR5 Receptor AntagonistsCell MovementCells, CulturedCyclohexanesCyclosporineHumansLipopolysaccharidesLungMaleMaravirocMiceMice, Inbred C57BLMice, KnockoutNeutrophilsCcr2 protein, mouseCCR5 Receptor AntagonistsCyclohexanesCyclosporinecyclosporin Hformyl peptide receptor 2, mouseFpr1 protein, mouseLipopolysaccharidesMaravirocReceptors, CCR2Receptors, CCR5Receptors, Formyl PeptideTriazoles

Identifiers

PMID23860188
PMCPMC6741509
OpenAlexW2061092156

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.