Evidence map›Paper›PMID 29089751›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2017

Characteristics and potential role of M2 macrophages in COPD.

Shengyang He, Lihua Xie, Junjuan Lu, Shenghua Sun

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. The potential role of 1,25(OH)Journal of inflammation (London, England) · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Lung Transcriptomics Link Emphysema to Barrier Dysfunction and Macrophage Subpopulations.American journal of respiratory and critical care medicine · 2025
    Article
  17. Article
  18. Review
  19. Review
  20. Article
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

4 authors at 2 institutions in 1 country.

Shengyang HeDepartment of Respiratory Medicine, The Third Xiangya Hospital of Central South University, Changsha, Hunan, People's Republic of China.
Lihua XieDepartment of Respiratory Medicine, The Third Xiangya Hospital of Central South University, Changsha, Hunan, People's Republic of China.
Junjuan LuDepartment of Respiratory Medicine, The Third Xiangya Hospital of Central South University, Changsha, Hunan, People's Republic of China.
Shenghua SunDepartment of Respiratory Medicine, The Third Xiangya Hospital of Central South University, Changsha, Hunan, People's Republic of China.
Third Xiangya Hospital · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCOPD is a multi-pathogenesis disease mainly caused by smoking. A further understanding of the mechanism of smoking-related COPD might contribute to preventions and treatments of this disease in the early stages. This study was designed to identify the characteristics of M2 macrophages in COPD for a better understanding about their potential role. MATERIALS AND

methodsCOPD models were built in the C57BL/6 mouse by cigarette smoke (CS) exposure combined with intraperitoneal injection of cigarette smoke extract (CSE). The modeling efficiency was evaluated by lung function and hematoxylin and eosin (H&E) staining. The number of different macrophage phenotypes was detected by immunohistochemical staining (IHS) of CD206, CD86 and CD68 on the lung tissue paraffin section. The RAW264.7 cells were polarized toward the M2 phenotype by interleukin IL-4 and confirmed by a flow cytometer. The gene expression levels of TGF-βRII, Smad2, Smad3 and Smad7 in CSE-treated M2 macrophages were detected by real-time reverse transcription polymerase chain reaction (RT-PCR). The expression levels of TGF-β/Smad pathway-related makers (TGF-βRII, p-Smad2, p-Smad3, Smad7 and TGF-β) in alveolar M2 macrophages were detected by two consecutive paraffin section IHS.

resultsThe COPD model is well established, which is confirmed by the lung function test and lung H&E staining. The whole number of macrophages and the ratio of M2/M1 phenotype are both increased (

conclusionThis study found an increased deposition of alveolar M2 macrophages in the mouse COPD model and an increased expression level of TGF-β/Smad pathway in M2 macrophages, both in vitro and in vivo, induced by CSE and/or CS exposure, indicating that M2 macrophages might contribute to COPD through changing of phenotype and TGF-β/Smad pathway.

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticB7-2 AntigenCD68 MoleculeDisease Models, AnimalInterleukin-4Lectins, C-TypeLungMacrophages, AlveolarMannose-Binding LectinsMannose ReceptorMiceMice, Inbred C57BLPhenotypePhosphorylationAntigens, CDAntigens, Differentiation, MyelomonocyticB7-2 AntigenCD68 MoleculeCD68 protein, mouseCd86 protein, mouseInterleukin-4Lectins, C-TypeMannose-Binding LectinsMannose ReceptorProtein Serine-Threonine KinasesReceptors, Cell SurfaceReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IISmad2 ProteinSmad2 protein, mouseSmad3 ProteinSmad3 protein, mouseSmad7 ProteinSmad7 protein, mouseCOPDM2 macrophageTGF-β/Smad pathway

Identifiers

PMID29089751
PMCPMC5655159
OpenAlexW2766885082

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.