Evidence map›Paper›PMID 34950055›Full record

ArticleFrontiers in physiology2021

The Heterogeneity of Inflammatory Response and Emphysema in Chronic Obstructive Pulmonary Disease.

Xia Xu, Ke Huang, Fen Dong, Shiwei Qumu, Qichao Zhao, Hongtao Niu, Xiaoxia Ren, Xiaoying Gu, Tao Yu, Lin Pan and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Article
  7. Article
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  9. SignallingERJ open research · 2025
    Article
  10. Article
  11. Article
  12. The persistent inflammation in COPD: is autoimmunity the core mechanism?European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Novel Anti-Inflammatory Approaches to COPD.International journal of chronic obstructive pulmonary disease · 2023
    Review
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 2 institutions in 1 country.

Xia XuDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Ke HuangDepartment of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Fen DongInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China.
Shiwei QumuDepartment of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Qichao ZhaoInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China.
Hongtao NiuDepartment of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Xiaoxia RenDepartment of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Xiaoying GuDepartment of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China.
Tao YuDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Lin PanInstitute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, China.
Ting YangDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Chen WangDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
China-Japan Friendship Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by chronic inflammation, emphysema, airway remodeling, and altered lung function. Despite the canonical classification of COPD as a neutrophilic disease, blood and airway eosinophilia are found in COPD patients. Identifying the tools to assess eosinophilic airway inflammation in COPD models during stable disease and exacerbations will enable the development of novel anti-eosinophilic treatments. We developed different animal models to mimic the pathological features of COPD. Our results show that eosinophils accumulated in the lungs of pancreatic porcine elastase-treated mice, with emphysema arising from the alveolar septa. A lipopolysaccharide challenge significantly increased IL-17 levels and induced a swift change from a type-2 response to an IL-17-driven inflammatory response. However, lipopolysaccharides can exacerbate cigarette smoking-induced airway inflammation dominated by neutrophil infiltration and airway remodeling in COPD models. Our results suggest that eosinophils may be associated with emphysema arising from the alveolar septa, which may be different from the small airway disease-associated emphysema that is dominated by neutrophilic inflammation in cigarette smoke-induced models. The characterization of heterogeneity seen in the COPD-associated inflammatory signature could pave the way for personalized medicine to identify new and effective therapeutic approaches for COPD.

Indexed as

chronic obstructive pulmonary diseaseemphysemaeosinophilsheterogeneityinflammation

Identifiers

PMID34950055
PMCPMC8689000
OpenAlexW4200059484

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.