ArticleImmunity, inflammation and disease2020
Six gene and TH2 signature expression in endobronchial biopsies of participants with asthma.
Article in Immunity, inflammation and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 14 citations in OpenAlex.
- Observational
- Using cell-specific late-phase asthma mRNA biomarkers to repurpose drugs that concurrently reverse disease signatures across multiple immune cell-types.PLoS computational biology · 2026Article
- Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Immune Training of the Interleukin 6 Gene in Airway Epithelial Cells is Central to Asthma Exacerbations.Allergy · 2026Article
- Multiomics and Machine Learning Reveal Distinct Immune-Metabolic Signatures and Diagnostic Biomarkers for Asthma Inflammatory Endotypes.ACS omega · 2025Article
- Identification and validation of differentially expressed genes in allergic asthma pathogenesis using whole-transcriptome sequencing.Frontiers in medicine · 2025Article
- SPIN: sex-specific and pathway-based interpretable neural network for sexual dimorphism analysis.Briefings in bioinformatics · 2024Article
- Article
- Pathways linked to unresolved inflammation and airway remodelling characterize the transcriptome in two independent severe asthma cohorts.Respirology (Carlton, Vic.) · 2022Article
- Construction of Severe Eosinophilic Asthma Related Competing Endogenous RNA Network by Weighted Gene Co-Expression Network Analysis.Frontiers in pharmacology · 2022Article
- A deoxyribonuclease 1-like 3 genetic variant associates with asthma exacerbations.The Journal of allergy and clinical immunology · 2021Article
- The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules.Frontiers in genetics · 2021Article
- Six gene and TH2 signature expression in endobronchial biopsies of participants with asthma.Immunity, inflammation and disease · 2020Article
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundBoth the six gene signature (6GS: CPA3, DNASE1L3, CLC, IL1B, ALPL, and CXCR2) and T-helper 2 signature (TH2S: CLCA1, SERPINB2, and POSTN) are proposed as biomarkers in the identification of inflammatory phenotypes of asthma in induced sputum and epithelial brushings, respectively. The aim of this study was to explore patterns of gene expression of known signatures, 6GS and TH2S in endobronchial biopsies.
methodsThis was an exploratory cross-sectional study of gene expression in endobronchial biopsies of 55 adults with asthma and 9 healthy controls (HC). The expression of the 6GS and TH2S was determined by quantitative polymerase chain reaction. Correlations with clinical and cellular characteristics were performed, and receiver operating characteristic was utilized to assess signatures' ability to predict asthma from HC and inflammatory phenotypes.
resultsGene expression of DNASE1L3 (P = .045) was upregulated in asthma compared with HC, and IL1B (P = .017) was upregulated in neutrophilic asthma compared with non-neutrophilic asthma. In asthma, the expression of CPA3 was negatively associated with ICS daily dose (r = -.339; P = .011), IL1B expression was positively associated with bronchial lavage fluid (BLF) total cell count (r = .340; P = .013) and both CLC and POSTN expression were associated with lymphocytes percentage in BLF (r = -.355, P = .009; r = -.300, P = .025, respectively). Both 6GS (area under curve [AUC] = 86.3%; P = .017) and TH2S (AUC = 72.7%; P = .037) could significantly predict asthma from HC. In addition, 6GS can identify neutrophilic (AUC = 93.2%; P = .005) and TH2S identifies eosinophilic (AUC = 62.7%; P = .033) asthma. CONCLUSIONS AND CLINICAL RELEVANCE: There was increased expression of DNASE1L3 in asthma and IL1B in neutrophilic asthma. These results show similar upregulated patterns of expression in two genes of the 6GS in endobronchial biopsies, previously identified in sputum. The upregulation of DNASE1L3 and IL1B suggests that common mechanisms may be at play throughout the airway.
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