Evidence map›Paper›PMID 16284650›Full record

ArticleThe Journal of clinical investigation2005

Role of CCR5 in IFN-gamma-induced and cigarette smoke-induced emphysema.

Bing Ma, Min-Jong Kang, Chun Geun Lee, Svetlana Chapoval, Wei Liu, Qingsheng Chen, Anthony J Coyle, José M Lora, Dominic Picarella, Robert J Homer and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 89 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Bing MaSection of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Min-Jong Kang
Chun Geun Lee
Svetlana Chapoval
Wei Liu
Qingsheng Chen
Anthony J Coyle
José M Lora
Dominic Picarella
Robert J Homer
Jack A Elias
Yale University · US

Funding

Unique role of lung dendritic cells in Th2 responsesP01HL056389 · NHLBI · YALE UNIVERSITY · PI COHN, LAUREN E · 2002 to 2006
$10.2M
TRANSGENIC MODELING OF AIRWAY INFLAMMATION IN ASTHMAP50HL056389 · NHLBI · YALE UNIVERSITY · PI REDLICH, CARRIE A · 1997 to 2001
$4.0M
Transgenic Modeling of TGF-Beta in the LungR01HL064242 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 1999 to 2007
$2.7M
VEGF in Th2 Inflammation and AsthmaR01HL078744 · NHLBI · YALE UNIVERSITY · PI ELIAS, JACK A · 2004 to 2008
$2.0M
NHLBI NIH HHS HL 064242NHLBI NIH HHS HL 078744NHLBI NIH HHS HL 56389NHLBI NIH HHS P01 HL056389NHLBI NIH HHS P50 HL056389NHLBI NIH HHS R01 HL064242NHLBI NIH HHS R01 HL078744
6 · The paper itself

Abstract

Th1 inflammation and remodeling characterized by tissue destruction frequently coexist in human diseases. To further understand the mechanisms of these responses, we defined the role(s) of CCR5 in the pathogenesis of IFN-gamma-induced inflammation and remodeling in a murine emphysema model. IFN-gamma was a potent stimulator of the CCR5 ligands macrophage inflammatory protein-1alpha/CCL-3 (MIP-1alpha/CCL-3), MIP-1beta/CCL-4, and RANTES/CCL-5, among others. Antibody neutralization or null mutation of CCR5 decreased IFN-gamma-induced inflammation, DNA injury, apoptosis, and alveolar remodeling. These interventions decreased the expression of select chemokines, including CCR5 ligands and MMP-9, and increased levels of secretory leukocyte protease inhibitor. They also decreased the expression and/or activation of Fas, FasL, TNF, caspase-3, -8, and -9, Bid, and Bax. In accordance with these findings, cigarette smoke induced pulmonary inflammation, DNA injury, apoptosis, and emphysema via an IFN-gamma-dependent pathway(s), and a null mutation of CCR5 decreased these responses. These studies demonstrate that IFN-gamma is a potent stimulator of CC and CXC chemokines and highlight the importance of CCR5 in the pathogenesis of IFN-gamma-induced and cigarette smoke-induced inflammation, tissue remodeling, and emphysema. They also demonstrate that CCR5 is required for optimal IFN-gamma stimulation of its own ligands, other chemokines, MMPs, caspases, and cell death regulators and the inhibition of antiproteases.

Indexed as

SmokingAnimalsAnnexin A5ApoptosisBronchoalveolar LavageCell DeathChemokinesDNADNA PrimersEmphysemaEnzyme-Linked Immunosorbent AssayFemaleImmunohistochemistryInflammationIn Situ Nick-End LabelingInterferon-gammaAnnexin A5ChemokinesDNADNA PrimersInterferon-gammaLigandsMatrix Metalloproteinase 9Receptors, CCR5RNA, Messenger

Identifiers

PMID16284650
PMCPMC1280966
OpenAlexW2151137229

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.