ArticleRespiratory research2026
The involvement of Th17 inflammation and miR-363-3p in airway epithelial barrier dysfunction.
Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Targeting Tight Junction Proteins to Restore Airway Epithelial Barrier Function in Asthma.Current allergy and asthma reports · 2026Review
- Neutrophilic asthma: advances in experimental models from pathogenesis to therapeutic translation.Molecular medicine (Cambridge, Mass.) · 2026Review
- Airway epithelial dysfunction in asthma pathogenesis: epigenetic mechanisms, inflammatory crosstalk, and therapeutic opportunities.Frontiers in allergy · 2026Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImpaired airway epithelial barrier function is a pathogenic driver in a subset of individuals with asthma. MicroRNAs, small RNAs that function as post-transcriptional regulators of gene expression, may be involved in the regulation of the airway epithelial barrier. This study aimed to determine if microRNAs cause epithelial barrier dysfunction through the targeting of mRNAs involved in maintaining airway epithelial barrier integrity.
methodsPrimary human bronchial epithelial cells cultured at air-liquid interface were stimulated with cytokines reflecting different asthma endotypes. Barrier integrity was assessed by FITC-labelled dextran flux. Differentially expressed epithelial barrier-related genes and microRNAs were identified by next-generation RNA sequencing and qPCR. Results were validated with microRNA pull-down, treatment with microRNA mimics and antagomirs, respectively, and evaluated in airway samples from subjects with asthma.
resultsA combination of IL-17A and TNFα, mimicking Th17 inflammation, was identified as a strong driver of epithelial barrier disruption, as compared to IL-4 + IL-13, IL-6 + sIL-6R, and TGFβ. Several microRNAs induced by IL-17A and TNFα stimulation were predicted to target barrier-related genes, which exhibited decreased expression in the same model. Of these microRNAs, miR-146a-3p and miR-363-3p were consistently induced in multiple donors. MicroRNA pull-down, overexpression, and knockdown experiments indicated a potential role for miR-363-3p interacting with several barrier-related genes, including CLDN8, PCDH1, and PTEN. Bronchial lavage samples demonstrated an increase of miR-363-3p in individuals with asthma compared to healthy controls, as well as a positive correlation between miR-363-3p and the number of airway eosinophils and neutrophils.
conclusionsOur results support the role of microRNAs as mediators of cytokine-induced airway epithelial barrier dysfunction. Specifically, miR-363-3p appears to contribute to epithelial damage by targeting and suppressing gene expressions of several key barrier components, including CLDN8, PCDH1, and PTEN, suggesting a novel role for this microRNA in Th17-driven airway disease. A better understanding of microRNA networks and their role in asthma pathogenesis may lead to novel biomarkers and therapeutic targets, which are currently needed for individuals with T2-low asthma and in Th17-driven asthma.
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