Evidence map›Paper›PMID 39793714›Full record

ArticleThe Journal of allergy and clinical immunology2025

Identification of bronchial epithelial genes associated with type 2 eosinophilic inflammation in asthma.

Stephane Esnault, Kimberly A Dill-McFarland, Matthew C Altman, Melissa A Rosenkranz, Nizar N Jarjour, William W Busse

Abstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Contemporary Concise Review 2025: Asthma.Respirology (Carlton, Vic.) · 2026
    Review
  2. 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.

Stephane EsnaultDivision of Allergy, Pulmonary and Critical Care Medicine, University of Wisconsin-Madison, Madison, Wis; University of Lille, INSERM, CHU Lille, U1286-INFINITE-Institute for Translational Research in Inflammation, Lille, France.
Kimberly A Dill-McFarlandDivision of Allergy and Infectious Diseases, University of Washington, Seattle, Wash.
Matthew C AltmanDivision of Allergy and Infectious Diseases, University of Washington, Seattle, Wash; Systems Immunology Program, Benaroya Research Institute, Seattle, Wash.
Melissa A RosenkranzCenter for Healthy Minds, University of Wisconsin-Madison, Madison, Wis; Department of Psychiatry, University of Wisconsin-Madison, Madison, Wis.
Nizar N JarjourDivision of Allergy, Pulmonary and Critical Care Medicine, University of Wisconsin-Madison, Madison, Wis.
William W BusseDivision of Allergy, Pulmonary and Critical Care Medicine, University of Wisconsin-Madison, Madison, Wis. Electronic address: wwb@medicine.wisc.edu.

Funding

University of Wisconsin Institute for Clinical and Translational ResearchUL1TR002373 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI ELIZABETH S BURNSIDE, Allan R. Brasier · 2017 to 2026
$75.9M
INSTITUTIONAL CTSA (UW-MADISON): CLINICAL TRIALSUL1RR025011 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2007 to 2011
$29.5M
Thr Role of Pin1 in AirwayP01HL088594 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI JARJOUR, NIZAR N · 2008 to 2017
$21.0M
Asthmatic Inflammation and Neurocircuitry ActivationR01HL123284 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI BUSSE, WILLIAM W. · 2016 to 2019
$2.9M
Investigating the mechanisms by which systemic inflammation promotes Alzheimer’s disease: Asthma as a model and modifiable risk factorRF1AG082215 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI JARJOUR, NIZAR N, ROSENKRANZ, MELISSA A · 2023 to 2023
$2.3M
NCATS NIH HHS UL1 TR002373NCRR NIH HHS UL1 RR025011NHLBI NIH HHS P01 HL088594NHLBI NIH HHS R01 HL123284NIA NIH HHS RF1 AG082215
6 · The paper itself

Abstract

backgroundAirway inflammation plays a critical role in asthma pathogenesis and pathophysiology, but the molecular pathways contributing to airway inflammation are not fully known, particularly type 2 (T2) inflammation characterized by both eosinophilia and higher fractional exhaled nitric oxide (Feno) levels.

objectiveWe sought to identify genes whose level of expression in epithelial brushing samples were associated with both bronchoalveolar lavage (BAL) eosinophilia and generation of Feno.

methodsWe performed segmental allergen bronchoprovocation (SBP-Ag) in participants with asthma, then RNA sequencing analyses of BAL cells and brushing samples before and 48 hours after SBP-Ag to identify regulation of eosinophil recruitment and Feno changes.

resultsAllergen bronchoprovocation increased Feno levels, which correlated with eosinophilia. Thirteen genes were identified in brushing samples, whose expression changed in response to SBP-Ag and correlated with both airway eosinophilia and Feno levels after SBP-Ag. Among these 13 genes, epithelial cell product CDH26/cadherin-26 contributed to the amplification of T2 inflammation, as reflected by eosinophilia and Feno, and causal mediation analyses with pro-T2 and proeosinophilic cytokine mediators in BAL fluids. Among the genes associated with reduced eosinophilia and Feno, HEY2 is known to enhance cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition, as well as to reduce apoptosis.

conclusionThis unbiased RNA sequencing analysis in participants with allergic asthma revealed several epithelial cell genes, particularly CDH26, that may be critical for the development or augmentation of T2 inflammation in asthma.

Indexed as

AsthmaBronchiEosinophiliaEosinophilsAdultBronchoalveolar Lavage FluidCadherinsEpithelial CellsFemaleHumansInflammationMaleMiddle AgedNitric OxideCadherinsNitric Oxideallergic challengeallergyAsthmabronchial brushingbronchoalveolar lavageCDH26eosinophilsmultiplex protein assaynitric oxideRNA sequencingtype 2 immune response

Identifiers

PMID39793714
PMCPMC12058426

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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.