Evidence map›Paper›PMID 22287613›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

A macrophage subpopulation recruited by CC chemokine ligand-2 clears apoptotic cells in noninfectious lung injury.

Jiurong Liang, Yoosun Jung, Robert M Tighe, Ting Xie, Ningshan Liu, Maura Leonard, Michael Dee Gunn, Dianhua Jiang, Paul W Noble

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

36 citing papers in PubMed, 57 citations in OpenAlex.

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  15. Macrophages in lung fibrosis.International immunology · 2021
    Review
  16. Article
  17. Airspace Macrophages and Monocytes Exist in Transcriptionally Distinct Subsets in Healthy Adults.American journal of respiratory and critical care medicine · 2021
    Article
  18. Article
  19. 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

9 authors at 1 institution in 1 country.

Jiurong LiangDivision of Pulmonary,Department of Medicine, Duke Univ. School of Medicine, Durham, NC 27710, USA.
Yoosun Jung
Robert M Tighe
Ting Xie
Ningshan Liu
Maura Leonard
Michael Dee Gunn
Dianhua Jiang
Paul W Noble
Duke University · US

Funding

MATRIX REGULATION OF FIBROPROLIFERATIVE LUNG DISEASEP50HL084917 · NHLBI · DUKE UNIVERSITY · PI WRIGHT, JO RAE · 2006 to 2010
$13.2M
MECHANISMS OF MACROPHAGE ACTIVATION IN LUNG INFLAMMATIONR01HL060539 · NHLBI · YALE UNIVERSITY · PI NOBLE, PAUL WESLEY · 1997 to 2019
$6.5M
Innate Immune Mechanisms of Non-infectious Lung InflammationR01AI052201 · NIAID · YALE UNIVERSITY · PI NOBLE, PAUL WESLEY · 2002 to 2021
$6.4M
Regulation of Pulmonary Fibrosis by CXCR3R01HL077291 · NHLBI · YALE UNIVERSITY · PI NOBLE, PAUL WESLEY · 2005 to 2013
$3.1M
Regulation of Lung Fibrosis by Alternatively Activated Macrophages and Arginase-1K08HL105537 · NHLBI · DUKE UNIVERSITY · PI TIGHE, ROBERT MATTHEW · 2012 to 2016
$492k
NHLBI NIH HHS K08 HL105537NHLBI NIH HHS P50 HL084917NHLBI NIH HHS P50-HL-084917NHLBI NIH HHS R01 HL060539NHLBI NIH HHS R01-HL-060539NHLBI NIH HHS R01 HL077291NHLBI NIH HHS R01-HL-077291NIAID NIH HHS R01 AI052201NIAID NIH HHS R01-AI-052201
6 · The paper itself

Abstract

CC chemokine ligand-2 (CCL2)/monocyte chemoattractant protein (MCP)-1 expression is upregulated during pulmonary inflammation, and the CCL2-CCR2 axis plays a critical role in leukocyte recruitment and promotion of host defense against infection. The role of CCL2 in mediating macrophage subpopulations in the pathobiology of noninfectious lung injury is unknown. The goal of this study was to examine the role of CCL2 in noninfectious acute lung injury. Our results show that lung-specific overexpression of CCL2 protected mice from bleomycin-induced lung injury, characterized by significantly reduced mortality, reduced neutrophil accumulation, and decreased accumulation of the inflammatory mediators IL-6, CXCL2 (macrophage inflammatory protein-2), and CXCL1 (keratinocyte-derived chemokine). There were dramatic increases in the recruitment of myosin heavy chain (MHC) II IA/IE(int)CD11c(int) cells, exudative macrophages, and dendritic cells in Ccl2 transgenic mouse lungs both at baseline and after bleomycin treatment compared with levels in wild-type mice. We further demonstrated that MHCII IA/IE(int)CD11c(int) cells engulfed apoptotic cells during acute lung injury. Our data suggested a previously undiscovered role for MHCII IA/IE(int)CD11c(int) cells in apoptotic cell clearance and inflammation resolution.

Indexed as

ApoptosisAcute Lung InjuryAnimalsBleomycinCD11c AntigenChemokine CCL2FemaleHumansInflammationInflammation MediatorsJurkat CellsLungMacrophagesMaleMiceMice, Inbred C57BLBleomycinCcr2 protein, mouseCD11c AntigenChemokine CCL2Inflammation MediatorsMyosin Heavy ChainsReceptors, CCR2

Identifiers

PMID22287613
PMCPMC3362164
OpenAlexW2060609132

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.