Evidence map›Paper›PMID 32824775›Full record

ReviewJournal of clinical medicine2020

Role of Type2 Inflammatory Biomarkers in Chronic Obstructive Pulmonary Disease.

Keiji Oishi, Kazuto Matsunaga, Toshihiro Shirai, Keita Hirai, Yasuhiro Gon

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-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

27 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Exacerbations and Healthcare Burden of COPD with Type 2 Inflammation: US Claims Analysis.International journal of chronic obstructive pulmonary disease · 2026
    Article
  5. Review
  6. Article
  7. Response.Chest · 2025
    Article
  8. The Burden of COPD with Type 2 Inflammation in North-West Continental Europe.International journal of chronic obstructive pulmonary disease · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 4 institutions in 1 country.

Keiji OishiDepartment of Medicine and Clinical Science, Graduate School of Medicine, Yamaguchi University, Yamaguchi 755-8505, Japan.ORCID 0000-0003-4230-0450
Kazuto MatsunagaDepartment of Respiratory Medicine and Infectious Disease, Graduate School of Medicine, Yamaguchi University, Yamaguchi 755-8505, Japan.ORCID 0000-0002-0514-3241
Toshihiro ShiraiDepartment of Respiratory Medicine, Shizuoka General Hospital, Shizuoka 420-8527, Japan.
Keita HiraiDepartment of Clinical Pharmacology and Genetics, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526, Japan.ORCID 0000-0001-8027-3508
Yasuhiro GonDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo 173-8601, Japan.ORCID 0000-0003-0514-3054
Yamaguchi University · JPNihon University · JPShizuoka General Hospital · JPUniversity of Shizuoka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway inflammation in chronic obstructive pulmonary disease (COPD) is typically thought to be driven by Type1 immune responses, while Type2 inflammation appears to be present in definite proportions in the stable state and during exacerbations. In fact, some COPD patients showed gene expression of Type2 inflammation in the airway, and this subset was associated with the inhaled corticosteroid (ICS) response. Interestingly enough, the relationship between COPD and diseases associated with Type2 inflammation from the perspective of impaired lung development is increasingly highlighted by recent epidemiologic studies on the origin of COPD. Therefore, many researchers have shown an interest in the prevalence and the role of existent Type2 biomarkers such as sputum and blood eosinophils, exhaled nitric oxide fraction, and atopy, not only in asthma but also in COPD. Although the evidence about Type2 biomarkers in COPD is inconsistent and less robust, Type2 biomarkers have shown some potential when analyzing various clinical outcomes or therapeutic response to ICS. In this article, we review the existent and emerging Type2 biomarkers with clinically higher applicability in the management of COPD.

Indexed as

airway inflammationasthma-chronic obstructive pulmonary disease overlapatopychitinase-3-like protein 1eosinophil-derived neurotoxineosinophilsfractional exhaled nitric oxideinhaled corticosteroid responseperiostin

Identifiers

PMID32824775
PMCPMC7464674
OpenAlexW3061501756

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.