Evidence map›Paper›PMID 21463523›Full record

ArticleFibrogenesis & tissue repair2011

Immune response CC chemokines CCL2 and CCL5 are associated with pulmonary sarcoidosis.

Vyacheslav Palchevskiy, Nastran Hashemi, Stephen S Weigt, Ying Ying Xue, Ariss Derhovanessian, Michael P Keane, Robert M Strieter, Michael C Fishbein, Jane C Deng, Joseph P Lynch and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Fibrogenesis & tissue repair, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 50 citations in OpenAlex.

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  15. Alveolar Macrophage ABCG1 Deficiency Promotes Pulmonary Granulomatous Inflammation.American journal of respiratory cell and molecular biology · 2019
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  18. Observational
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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

12 authors at 4 institutions in 2 countries.

Vyacheslav Palchevskiy *Division of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Nastran Hashemi *Division of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Stephen S WeigtDivision of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Ying Ying XueDivision of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Ariss DerhovanessianDivision of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Michael P KeaneDepartment of Medicine, St Vincent's University Hospital and University College Dublin, Dublin, Ireland.
Robert M StrieterDivision of Pulmonary and Critical Care Medicine, Department of Medicine, University of Virginia Health System, Charlottesville, VA, USA.
Michael C FishbeinDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Jane C DengDivision of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Joseph P LynchDivision of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Robert ElashoffDepartment of Biomathematics, UCLA, Los Angeles, CA, USA.
John A BelperioDivision of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
University of California, Los Angeles · USApplied Biomathematics (United States) · USUniversity College Dublin · IEUniversity of Virginia Health System · US

Funding

Role of IRAK-M in sepsis-induced immunosuppressionK08HL081229 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DENG, JANE C · 2005 to 2010
$609k
NHLBI NIH HHS K08 HL081229
6 · The paper itself

Abstract

backgroundPulmonary sarcoidosis involves an intense leukocyte infiltration of the lung with the formation of non-necrotizing granulomas. CC chemokines (chemokine (C-C motif) ligand 2 (CCL2)-CCL5) are chemoattractants of mononuclear cells and act through seven transmembrane G-coupled receptors. Previous studies have demonstrated conflicting results with regard to the associations of these chemokines with sarcoidosis. In an effort to clarify previous discrepancies, we performed the largest observational study to date of CC chemokines in bronchoalveolar lavage fluid (BALF) from patients with pulmonary sarcoidosis.

resultsBALF chemokine levels from 72 patients affected by pulmonary sarcoidosis were analyzed by enzyme-linked immunosorbent assay (ELISA) and compared to 8 healthy volunteers. BALF CCL3 and CCL4 levels from pulmonary sarcoidosis patients were not increased compared to controls. However, CCL2 and CCL5 levels were elevated, and subgroup analysis showed higher levels of both chemokines in all stages of pulmonary sarcoidosis. CCL2, CCL5, CC chemokine receptor type 1 (CCR1), CCR2 and CCR3 were expressed from mononuclear cells forming the lung granulomas, while CCR5 was only found on mast cells.

conclusionsThese data suggest that CCL2 and CCL5 are important mediators in recruiting CCR1, CCR2, and CCR3 expressing mononuclear cells as well as CCR5-expressing mast cells during all stages of pulmonary sarcoidosis.

Identifiers

PMID21463523
PMCPMC3080805
OpenAlexW2101317551

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Registered trials

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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.