Evidence map›Paper›PMID 39534492›Full record

ReviewBreathe (Sheffield, England)2024

Type 2 inflammation in COPD: is it just asthma?

Augusta Beech, Andrew Higham, Sophie Booth, Vickram Tejwani, Frederik Trinkmann, Dave Singh

Abstract readReview
In one paragraph

Review in Breathe (Sheffield, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
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  5. Observational
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  9. Article
  10. Review
  11. Eosinophils in chronic obstructive pulmonary disease.Therapeutic advances in respiratory disease
    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

6 authors.

Augusta BeechDivision of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK.ORCID https://orcid.org/0000-0002-2690-5364
Andrew HighamDivision of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK.ORCID https://orcid.org/0000-0002-8094-3505
Sophie BoothDivision of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK.
Vickram TejwaniDepartment of Pulmonary Medicine, Integrated Hospital Care Institute, Cleveland Clinic, Cleveland, OH, USA.
Frederik TrinkmannDepartment of Pneumology and Critical Care Medicine, Thoraxklinik at Heidelberg University Hospital, Translational Lung Research Center Heidelberg, German Center for Lung Research (DZL), Heidelberg, Germany.ORCID https://orcid.org/0000-0001-5877-877X
Dave SinghDivision of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester and Manchester University NHS Foundation Trust, Manchester, UK.

Funding

Leukotriene B4 and IL-8 in alpha-1 heterozygotes (PI*MZ genotype)K23HL173570 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI Vickram Tejwani · 2024 to 2026
$512k
NHLBI NIH HHS K23 HL173570
6 · The paper itself

Abstract

COPD is a heterogeneous condition, with tobacco smoking being the main environmental risk factor. The presence of type 2 (T2) inflammation is a well-recognised feature of asthma; however, it is now apparent that a subset of COPD patients also displays evidence of T2 inflammation with respect to elevated eosinophil counts and altered gene and protein expression of several T2 inflammatory mediators. T2 inflammatory mediators represent an attractive therapeutic target in both COPD and asthma; however, the efficacy of pharmaceutical interventions varies between diseases. Furthermore, the nature of some shared clinical features also differs. We provide a narrative review of differences in the nature of T2 inflammation between COPD and asthma, which may partly explain phenotypic differences between diseases. We focus on evidence from studies of pulmonary histopathology, sputum and epithelial gene and protein expression, and response to pharmacological interventions targeted at T2 inflammation.

Identifiers

PMID39534492
PMCPMC11555586

What OpenQuestion holds

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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.