Evidence map›Paper›PMID 42473711›Full record

ArticleAllergy2026

The Airway Transcriptome in Type 2 Cytokine Biomarker-High and -Low Severe Asthma.

Jiashu Shen, Rekha Chaudhuri, Stephen Bicknell, Adel H Mansur, Rahul Shrimanker, Ian D Pavord, Stephen J Fowler, Vanessa Brown, Lorcan P McGarvey, Peter H Howarth and 10 more

Abstract read
In one paragraph

Article in Allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

20 authors.

Jiashu ShenNIHR Oxford Respiratory BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.ORCID https://orcid.org/0000-0003-0176-0274
Rekha ChaudhuriGartnavel General Hospital, Glasgow, and Institute of Infection& Immunity, University of Glasgow, Glasgow, UK.
Stephen BicknellGartnavel General Hospital, Glasgow, and Institute of Infection& Immunity, University of Glasgow, Glasgow, UK.
Adel H MansurUniversity of Birmingham and Heartlands Hospital, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.
Rahul ShrimankerNIHR Oxford Respiratory BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Ian D PavordNIHR Oxford Respiratory BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Stephen J FowlerSchool of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre and NIHR Manchester Biomedical Research Centre, Manchester University Hospitals NHS Foundation Trust, Manchester, UK.
Vanessa BrownWellcome-Wolfson- Centre for Experimental Medicine, Queen's University Belfast School of Medicine, Dentistry and Biomedical Sciences, Belfast, UK.
Lorcan P McGarveyWellcome-Wolfson- Centre for Experimental Medicine, Queen's University Belfast School of Medicine, Dentistry and Biomedical Sciences, Belfast, UK.
Peter H HowarthSchool of Clinical and Experimental Sciences, University of Southampton, NIHR Southampton Biomedical Research Centre, Southampton, UK.
Sven-Erik DahlénDepartment of Medicine, Huddinge, and, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Ian M AdcockNational Heart and Lung Institute, Imperial College, London, UK.ORCID https://orcid.org/0000-0003-2101-8843
Nazanin Zounemat-KermaniNational Heart and Lung Institute, Imperial College, London, UK.ORCID https://orcid.org/0000-0003-2479-3861
Joseph R ArronGenentech, Inc, South San Francisco, California, USA.
Liam G HeaneyWellcome-Wolfson- Centre for Experimental Medicine, Queen's University Belfast School of Medicine, Dentistry and Biomedical Sciences, Belfast, UK.
David F ChoyGenentech, Inc, South San Francisco, California, USA.
Timothy S C HinksNIHR Oxford Respiratory BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.ORCID https://orcid.org/0000-0003-0699-2373
Emanuele MarchiNIHR Oxford Respiratory BRC, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Peter BraddingDepartment of Respiratory Sciences, University of Leicester, NIHR Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, UK.
UK Medical Research Council Refractory Asthma Stratification programme (RASP‐UK)

Funding

MRC Stratified Medicine MR/M016579/1Wellcome TrustWellcome Trust 211050/Z/18/z
6 · The paper itself

Abstract

Severe asthma is a heterogeneous disease. The mechanisms driving airway pathology when type 2 (T2) cytokine activity is suppressed remain poorly understood. This study aimed to provide insight by identifying the airway molecular pathways of T2 biomarker-high and -low severe asthma. We analysed clinical and transcriptomic data from bronchial biopsies and brushes in the UK Refractory Asthma Stratification Programme multi-centre severe asthma cohort (18 corticosteroid-resistant T2 biomarker-high [T2-high], 23 T2 biomarker-intermediate [T2-intermediate], 11 T2 biomarker-low [T2-low]) plus 20 healthy controls pre- and post-treatment with high-dose inhaled corticosteroids (ICS). Many genes dysregulated in asthma vs. health were concordantly dysregulated in healthy subjects receiving ICS. Severe asthma as a whole, independent of confounding by ICS, was characterised by upregulation of mucins, CEACAM5, typical T2-genes (POSTN, CLCA1, CCL26), epithelial mast cell genes, and CPA4. T2-high severe asthma demonstrated upregulated T2-dependent genes, epithelial barrier and keratin genes, adaptive immune responses, and impaired ciliary function. T2-low asthma showed upregulated Th1- and IL-17-associated genes (IDO1, CXCL10, GBP1, LAG3), interferon-γ signalling, neuroimmune pathways, airway smooth muscle-related genes, and neutrophil enrichment. T2-intermediate asthma exhibited a mixed molecular profile sharing features of T2-high and T2-low endotypes, with selective expression of the pathogen defence and antiviral response genes. The results were validated using bronchoscopy data from the U-BIOPRED Consortium. This study defines airway molecular endotypes of severe asthma associated with T2 biomarker high and low phenotypes, independent of corticosteroid effects. These findings offer insights for severe asthma management and the development of targeted biologic therapies.

Indexed as

AsthmaCytokinesTh2 CellsTranscriptomeAdultBiomarkersFemaleGene Expression ProfilingHumansMaleMiddle AgedSeverity of Illness IndexBiomarkersCytokinescorticosteroid resistancemechanismsremodellingsevere asthmatranscriptome

Identifiers

PMID42473711
PMCPMC13569630

What OpenQuestion holds

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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.