ArticleClinical and translational allergy2025
Type 2 gene expression signature in severe asthma associates with more advanced airway remodeling.
Article in Clinical and translational allergy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- Effect of bronchial thermoplasty on airway inflammatory and profibrotic gene expression after one-year follow-up in severe asthma.Frontiers in immunology · 2026Article
- LYVE-1 identifies asthma and drives PDGF-BB-induced proliferation, migration, and oxidative stress in airway smooth muscle cells via the PI3K/Akt pathway.Frontiers in pharmacology · 2026Article
- Review
- Distinct Phenotypes of Peripheral Innate Lymphoid Cells and T Cells in Type 2 and Non-Type 2 Asthma.Clinical and translational allergy · 2025Article
- Type 2 gene expression signature in severe asthma associates with more advanced airway remodeling.Clinical and translational allergy · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundAsthma is a heterogeneous disease with various inflammatory subtypes, including the type-2 (T2) endotype associated with airway eosinophilia. Severe asthma is linked to reduced ventilatory function due to airway structural changes. This study compared the extent of airway remodeling in different immunological endotypes of asthma.
methodsSevere asthma patients (n = 30) were stratified based on bronchial expression of T2 (e.g., CST1) and T3 (e.g., IL17A) immunity genes as T2-high, T3-high, or low-inflammatory. We analyzed airway wall thickness using endobronchial ultrasound (EBUS), bronchial biopsy morphometry, and mRNA expression of remodeling genes. Bronchial epithelial cell cultures were used to assess cytokine responses.
resultsT2-high asthma patients showed lower predicted FEV1 (59 vs. 74 % in low-inflammatory variant, p = 0.049) and increased submucosa layer (L2) in EBUS (0.203 vs. 0.189 mm, p = 0.018). T2-high asthma patients also had increased airway smooth muscle (ASM) mass (∼2-fold, p = 0.018) and marginally thicker reticular basement membrane. T3-high asthma showed only a trend toward thicker L2 (p = 0.055). Only patients with an eosinophilic signature in endobronchial biopsy demonstrated increased expression of remodeling genes, including TGFB1. A profibrotic profile was also induced in bronchial epithelium stimulated in vitro with IL-13.
conclusionThese data suggest that T2-signature in severe asthma is associated with increased ASM mass and more pronounced airway obstruction. Overexpression of remodeling genes primarily occurred in patients with signs of eosinophilic infiltration in the bronchial mucosa, suggesting that remodeling may progress with uncontrolled airway inflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.