ArticleAllergy2015
eQTL of bronchial epithelial cells and bronchial alveolar lavage deciphers GWAS-identified asthma genes.
Article in Allergy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 103 citations in OpenAlex.
- Decreased sphingolipid synthesis in children with 17q21 asthma-risk genotypes.The Journal of clinical investigation · 2020Trial
- Histidine metabolic reprogramming drives oxidative stress induced mtDNA release to promote necroptosis and airway inflammation in severe asthma.Redox biology · 2026Article
- AI-based prediction of aspirin-exacerbated respiratory disease using nasal epithelial mRNA expression profiles.The journal of allergy and clinical immunology. Global · 2026Article
- Mechanisms and therapeutic strategies of asthma: from bench to bedside.Signal transduction and targeted therapy · 2026Review
- Tonsillar expression quantitative trait loci verify and expand genetic contributors to childhood atopic diseases.bioRxiv : the preprint server for biology · 2026Article
- Genome-wide Association Study IdentifiesAllergy, asthma & immunology research · 2026Article
- Genetic Background of Eosinophilic Esophagitis and Esophageal Atresia in Children.Digestive diseases and sciences · 2025Article
- Innate Immunity and Asthma Exacerbations: Insights From Human Models.Immunological reviews · 2025Review
- Potential drug targets for asthma identified through mendelian randomization analysis.Respiratory research · 2025Article
- Exploring the molecular mechanisms of asthma across multiple datasets.Annals of medicine · 2024Article
- The genetic regulation of the gastric transcriptome is associated with metabolic and obesity-related traits and diseases.Physiological genomics · 2024Article
- Exploring TSLP and IL-33 Serum Levels and Genetic Variants: Unveiling Their Limited Potential as Biomarkers for Mild Asthma in Children.Journal of clinical medicine · 2024Article
- Effect of air pollution on asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2024Review
- IL-33 Expression Is Lower in Current Smokers at both Transcriptomic and Protein Levels.American journal of respiratory and critical care medicine · 2023Article
- Genetic analyses of chr11p15.5 region identifyThe Journal of asthma : official journal of the Association for the Care of Asthma · 2023Article
- Single‑nucleotide polymorphism rs6592645 confers asthma risk through regulatingExperimental and therapeutic medicine · 2023Article
- Proline is increased in allergic asthma and promotes airway remodeling.JCI insight · 2023Article
- Th2 high and mast cell gene signatures are associated with corticosteroid sensitivity in COPD.Thorax · 2023Article
- Low CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity.American journal of respiratory and critical care medicine · 2023Article
- Airway remodeling heterogeneity in asthma and its relationship to disease outcomes.Frontiers in physiology · 2023Review
4 more citing papers are in PubMed but not listed here.
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 at 5 institutions in 1 country.
Funding
Abstract
backgroundGenome-wide association studies (GWASs) have identified various genes associated with asthma, yet, causal genes or single nucleotide polymorphisms (SNPs) remain elusive. We sought to dissect functional genes/SNPs for asthma by combining expression quantitative trait loci (eQTLs) and GWASs.
methodsCis-eQTL analyses of 34 asthma genes were performed in cells from human bronchial epithelial biopsy (BEC, n = 107) and from bronchial alveolar lavage (BAL, n = 94).
resultsFor TSLP-WDR36 region, rs3806932 (G allele protective against eosinophilic esophagitis) and rs2416257 (A allele associated with lower eosinophil counts and protective against asthma) were correlated with decreased expression of TSLP in BAL (P = 7.9 × 10(-11) and 5.4 × 10(-4) , respectively) and BEC, but not WDR36. Surprisingly, rs1837253 (consistently associated with asthma) showed no correlation with TSLP expression levels. For ORMDL3-GSDMB region, rs8067378 (G allele protective against asthma) was correlated with decreased expression of GSDMB in BEC and BAL (P = 1.3 × 10(-4) and 0.04) but not ORMDL3. rs992969 in the promoter region of IL33 (A allele associated with higher eosinophil counts and risk for asthma) was correlated with increased expression of IL33 in BEC (P = 1.3 × 10(-6) ) but not in BAL.
conclusionsOur study illustrates cell-type-specific regulation of the expression of asthma-related genes documenting SNPs in TSLP, GSDMB, IL33, HLA-DQB1, C11orf30, DEXI, CDHR3, and ZBTB10 affect asthma risk through cis-regulation of its gene expression. Whenever possible, disease-relevant tissues should be used for transcription analysis. SNPs in TSLP may affect asthma risk through up-regulating TSLP mRNA expression or protein secretion. Further functional studies are warranted.
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.