Evidence map›Paper›PMID 24498098›Full record

ArticlePloS one2014

Overexpression of CD163, CD204 and CD206 on alveolar macrophages in the lungs of patients with severe chronic obstructive pulmonary disease.

Yoichiro Kaku, Haruki Imaoka, Yoshitaka Morimatsu, Yoshihiro Komohara, Koji Ohnishi, Hanako Oda, Shinichi Takenaka, Masanobu Matsuoka, Tomotaka Kawayama, Motohiro Takeya and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

94 citing papers in PubMed, 152 citations in OpenAlex.

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34 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Yoichiro KakuDivision of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Haruki ImaokaDivision of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Yoshitaka MorimatsuDivision of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Yoshihiro KomoharaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Koji OhnishiDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Hanako OdaDivision of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Shinichi TakenakaDivision of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Masanobu MatsuokaDivision of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Tomotaka KawayamaDivision of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Motohiro TakeyaDepartment of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Tomoaki HoshinoDivision of Respirology, Neurology, and Rheumatology, Department of Medicine 1, Kurume University School of Medicine, Kurume, Fukuoka, Japan.
Kurume University · JPKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously reported that the lungs of patients with very severe chronic obstructive pulmonary disease (COPD) contain significantly higher numbers of alveolar macrophages than those of non-smokers or smokers. M1 and M2 macrophages represent pro- and anti-inflammatory populations, respectively. However, the roles of M1 and M2 alveolar macrophages in COPD remain unclear. Immunohistochemical techniques were used to examine CD163, CD204 and CD206, as M2 markers, expressed on alveolar macrophages in the lungs of patients with mild to very severe COPD (Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I (mild) n = 11, II (moderate) n = 9, III (severe) n = 2, and IV (very severe) n = 16). Fifteen smokers and 10 non-smokers were also examined for comparison. There were significantly higher numbers of alveolar macrophages in COPD patients than in smokers and non-smokers. The numbers and percentages of CD163(+), CD204(+) or CD206(+) alveolar macrophages in patients with COPD at GOLD stages III and IV were significantly higher than in those at GOLD stages I and II, and those in smokers and non-smokers. In patients with COPD, there was a significant negative correlation between the number of CD163(+), CD204(+) or CD206(+) alveolar macrophages and the predicted forced expiratory volume in one second. Overexpression of CD163, CD204 and CD206 on lung alveolar macrophages may be involved in the pathogenesis of COPD.

Indexed as

AgedAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenFemaleHumansLectins, C-TypeLungMacrophages, AlveolarMaleMannose-Binding LectinsMannose ReceptorMatrix Metalloproteinase 9Middle AgedPulmonary AlveoliPulmonary Disease, Chronic ObstructiveAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenLectins, C-TypeMannose-Binding LectinsMannose ReceptorMatrix Metalloproteinase 9MSR1 protein, humanReceptors, Cell SurfaceScavenger Receptors, Class A

Identifiers

PMID24498098
PMCPMC3907529
OpenAlexW1972872876

What OpenQuestion holds

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LicenceCC BY
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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.