Evidence map›Paper›PMID 33859282›Full record

ArticleScientific reports2021

Macrophages with reduced expressions of classical M1 and M2 surface markers in human bronchoalveolar lavage fluid exhibit pro-inflammatory gene signatures.

Hiroto Takiguchi, Chen X Yang, Cheng Wei Tony Yang, Basak Sahin, Beth A Whalen, Stephen Milne, Kentaro Akata, Kei Yamasaki, Julia Shun Wei Yang, Chung Yan Cheung and 8 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Preclinical models of COPD: a state of the art review.The European respiratory journal · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  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

18 authors at 3 institutions in 3 countries.

Hiroto TakiguchiSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Chen X YangSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Cheng Wei Tony YangSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Basak SahinSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Beth A WhalenSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Stephen MilneSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Kentaro AkataSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Kei YamasakiSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Julia Shun Wei YangSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Chung Yan CheungSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Ryan Vander WerffThe Biomedical Research Centre, University of British Columbia, Vancouver, BC, Canada.
Kelly M McNagnyThe Biomedical Research Centre, University of British Columbia, Vancouver, BC, Canada.
Fernando Sergio Leitao FilhoSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Tawimas ShaipanichDivision of Respiratory Medicine, UBC Department of Medicine, Vancouver, BC, Canada.
Stephan F van EedenSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Ma'en ObeidatSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Janice M LeungSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada.
Don D SinSt Paul's Hospital, The University of British Columbia (UBC) Centre for Heart Lung Innovation (HLI), Vancouver, BC, Canada. don.sin@hli.ubc.ca.
St. Paul's Hospital · CAUniversity of British Columbia · CAUniversity of British Columbia Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The classical M1/M2 polarity of macrophages may not be applicable to inflammatory lung diseases including chronic obstructive pulmonary disease (COPD) due to the complex microenvironment in lungs and the plasticity of macrophages. We examined macrophage sub-phenotypes in bronchoalveolar lavage (BAL) fluid in 25 participants with CD40 (a M1 marker) and CD163 (a M2 marker). Of these, we performed RNA-sequencing on each subtype in 10 patients using the Illumina NextSeq 500. Approximately 25% of the macrophages did not harbor classical M1 or M2 surface markers (double negative, DN), and these cells were significantly enriched in COPD patients compared with non-COPD patients (46.7% vs. 14.5%, p < 0.001). 1886 genes were differentially expressed in the DN subtype compared with  all other subtypes at a 10% false discovery rate. The 602 up-regulated genes included 15 mitochondrial genes and were enriched in 86 gene ontology (GO) biological processes including inflammatory responses. Modules associated with cellular functions including oxidative phosphorylation were significantly down-regulated in the DN subtype. Macrophages in the human BAL fluid, which were negative for both M1/M2 surface markers, harbored a gene signature that was pro-inflammatory and suggested dysfunction in cellular homeostasis. These macrophages may contribute to the pathogenesis and manifestations of inflammatory lung diseases such as COPD.

Indexed as

Antigens, CDAntigens, Differentiation, MyelomonocyticAntigens, SurfaceCD40 AntigensMacrophagesReceptors, Cell SurfaceBronchoalveolar Lavage FluidCD163 AntigenHomeostasisHumansInflammationOxidative PhosphorylationPulmonary Disease, Chronic ObstructiveAntigens, CDAntigens, Differentiation, MyelomonocyticAntigens, SurfaceCD163 AntigenCD40 AntigensReceptors, Cell Surface

Identifiers

PMID33859282
PMCPMC8050093
OpenAlexW3153145623

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.