Evidence map›Paper›PMID 35537820›Full record

ArticleThorax2023

Mendelian randomisation of eosinophils and other cell types in relation to lung function and disease.

Anna Guyatt, Catherine John, Alexander T Williams, Nick Shrine, Nicola F Reeve, SpiroMeta consortium, Ian Sayers, Ian Hall, Louise V Wain, Nuala Sheehan and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Thorax, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Plasma Levels of CXCL9 and MCP-3 are Increased in Asthma-COPD Overlap (ACO) Patients.International journal of chronic obstructive pulmonary disease · 2025
    Article
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  8. Article
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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 2 countries.

Anna GuyattDepartment of Health Sciences, University of Leicester, Leicester, UK.ORCID 0000-0003-1860-6337
Catherine JohnDepartment of Health Sciences, University of Leicester, Leicester, UK cj153@leicester.ac.uk.ORCID 0000-0002-6057-2073
Alexander T WilliamsDepartment of Health Sciences, University of Leicester, Leicester, UK.
Nick ShrineDepartment of Health Sciences, University of Leicester, Leicester, UK.ORCID 0000-0003-3641-4371
Nicola F ReeveDepartment of Health Sciences, University of Leicester, Leicester, UK.
SpiroMeta consortium
Ian SayersDivision of Respiratory Medicine, University of Nottingham, Nottingham, UK.
Ian HallDivision of Respiratory Medicine, University of Nottingham, Nottingham, UK.ORCID 0000-0001-9933-3216
Louise V WainDepartment of Health Sciences, University of Leicester, Leicester, UK.
Nuala SheehanDepartment of Health Sciences, University of Leicester, Leicester, UK.
Frank DudbridgeDepartment of Health Sciences, University of Leicester, Leicester, UK.
Martin D TobinDepartment of Health Sciences, University of Leicester, Leicester, UK.
University of Leicester · GBUniversity of Nottingham · GB

Funding

British Heart Foundation AA/18/3/34220Medical Research Council MC_PC_17228Medical Research Council MC_PC_19004Medical Research Council MC_QA137853Medical Research Council MR/N011317/1Medical Research Council MR/P00167X/1Medical Research Council MR/S037055/1Wellcome Trust
6 · The paper itself

Abstract

rationaleEosinophils are associated with airway inflammation in respiratory disease. Eosinophil production and survival is controlled partly by interleukin-5: anti-interleukin-5 agents reduce asthma and response correlates with baseline eosinophil counts. However, whether raised eosinophils are causally related to chronic obstructive pulmonary disease (COPD) and other respiratory phenotypes is not well understood.

objectivesWe investigated causality between eosinophils and: lung function, acute exacerbations of COPD, asthma-COPD overlap (ACO), moderate-to-severe asthma and respiratory infections.

methodsWe performed Mendelian randomisation (MR) using 151 variants from genome-wide association studies of blood eosinophils in UK Biobank/INTERVAL, and respiratory traits in UK Biobank/SpiroMeta, using methods relying on different assumptions for validity. We performed multivariable analyses using eight cell types where there was possible evidence of causation by eosinophils. MEASUREMENTS AND MAIN

resultsCausal estimates derived from individual variants were highly heterogeneous, which may arise from pleiotropy. The average effect of raising eosinophils was to increase risk of ACO (weighted median OR per SD eosinophils, 1.44 (95%CI 1.19 to 1.74)), and moderate-severe asthma (weighted median OR 1.50 (95%CI 1.23 to 1.83)), and to reduce forced expiratory volume in 1 s (FEV

conclusionsBroad consistency across MR methods may suggest causation by eosinophils (although of uncertain magnitude), yet heterogeneity necessitates caution: other important mechanisms may be responsible for the impairment of respiratory health by these eosinophil-raising variants. These results could suggest that anti-IL5 agents (designed to lower eosinophils) may be valuable in treating other respiratory conditions, including people with overlapping features of asthma and COPD.

Indexed as

AsthmaPulmonary Disease, Chronic ObstructiveEosinophilsForced Expiratory VolumeGenome-Wide Association StudyHumansLungAsthma EpidemiologyAsthma GeneticsAsthma MechanismsCOPD epidemiologyCOPD exacerbations mechanismsEosinophil BiologyRespiratory Infection

Identifiers

PMID35537820
PMCPMC10176352
OpenAlexW4280626259

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.