Evidence map›Paper›PMID 41805075›Full record

ArticleAllergy2026

Nasal Airway Transcriptome Reflects Selected Asthma-Associated Gene Signatures in the Lower Airways.

Hui Wen, Tessa Kole, Orestes A Carpaij, Tatiana Karp, Victor Guryev, Alen Faiz, Kian Fan Chung, Pankaj Bhavsar, Ian M Adcock, Salman Siddiqui and 13 more

Abstract read
PubMed Full text at PMC Publisher
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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

23 authors.

Hui WenGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0009-0003-0370-0459
Tessa KoleGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Orestes A CarpaijGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Tatiana KarpGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0009-0003-6435-4545
Victor GuryevGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Alen FaizGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Kian Fan ChungNational Heart and Lung Institute, Imperial College London, London, UK.ORCID https://orcid.org/0000-0001-7101-1426
Pankaj BhavsarNational Heart and Lung Institute, Imperial College London, London, UK.
Ian M AdcockNational Heart and Lung Institute, Imperial College London, London, UK.ORCID https://orcid.org/0000-0003-2101-8843
Salman SiddiquiNational Heart and Lung Institute, Imperial College London, London, UK.ORCID https://orcid.org/0000-0003-3770-7870
Andy LanGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0009-0003-2260-1894
Katie L RabyNational Heart and Lung Institute, Imperial College London, London, UK.
Nazanin Zounemat-KermaniData Science Institute, Imperial College London, London, UK.
Chris BrightlingInstitute for Lung Health, National Institute for Health and Care Research, Leicester Biomedical Research Centre, Department of Respiratory Sciences, University of Leicester, Leicester, UK.
Dave SinghCentre for Respiratory Medicine and Allergy, Manchester University NHS Foundation Trust, University of Manchester, Manchester, UK.
Janwillem KocksGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Monica KraftSamuel Bronfman Department of Medicine, Icahn School of Medicine, Mount Sinai Medical Center, New York, USA.
Bianca BeghéDepartment of Respiratory Diseases, University of Modena and Reggio Emilia, Modena, Italy.
Klaus F RabeDepartment of Medicine, Christian Albrechts University Kiel, Kiel and Lungen Clinic, Grosshansdorf, Germany.ORCID https://orcid.org/0000-0002-7020-1401
Alberto PapiSection of Respiratory Medicine, Department of Translational Medicine, University of Ferrara, Ferrara, Italy.ORCID https://orcid.org/0000-0002-6924-4500
Machteld N HylkemaGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Martijn C NawijnGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Maarten van den BergeGroningen Research Institute for Asthma and COPD, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.

Funding

Dutch Foundation for Asthma PreventionDutch Ministry of Health via the Public-Private Partnership ProgramGlaxoSmithKline
6 · The paper itself

Abstract

backgroundTranscriptomic analysis of bronchial brushes reveals asthma-associated gene signatures but is limited by the invasiveness of bronchoscopy. Based on the "united airways" hypothesis, we evaluated whether and to what extent nasal brushes reflect asthma-associated transcriptomic changes in the lower airways.

methodsIn the ARMS study, we included 26 asthma patients and 28 healthy controls, all fully clinically characterized. Nasal and bronchial brushes were collected for RNA sequencing. We used edgeR and WGCNA to identify asthma-associated genes and modules in bronchial brushes. We assessed their expression patterns in ARMS nasal brushes and validated the findings in the independent ATLANTIS study (n = 427).

resultsWe identified 51 asthma-associated genes in the lower airways, of which 40 were up-regulated and 11 were down-regulated in asthma compared to healthy controls. Seven of the 40 up-regulated genes were also up-regulated in ARMS nasal brushes and validated in ATLANTIS: CLCA1, FETUB, CST1, NTRK2, CDH26, TPSAB1, and DHX35. WGCNA revealed two modules that were consistently elevated in asthma across bronchial and nasal brushes in ARMS and confirmed in ATLANTIS. One module represents IL-13 related inflammation, whereas the other represents mast cell activity.

conclusionThe asthma-associated gene signatures of the lower and upper airways show a limited but biologically coherent overlap, with seven genes and two gene modules consistently elevated in asthma. The shared gene signatures reflect two separate components of type 2 inflammation: IL-13 related inflammation and mast cell activity. Selected nasal gene signatures offer a non-invasive tool to identify asthma endotypes with distinct molecular mechanisms driving underlying disease biology.

Indexed as

AsthmaBronchiNasal MucosaTranscriptomeAdultBiomarkersFemaleGene Expression ProfilingHumansMaleMiddle AgedBiomarkersasthmaIL‐13 related inflammationnon‐invasivetype 2 inflammationunited airways

Identifiers

PMID41805075
PMCPMC13569660

What Socratic holds

Textmetadata
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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 Socratic graph.