ArticleAsia Pacific allergy2020
DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins.
Article in Asia Pacific allergy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Hypoxia disrupts human bronchial epithelial barrier integrity via tight junction protein remodeling and enhanced paracellular leakage.European journal of medical research · 2025Article
- The inhibitory effects of live and UV-killed Akkermansia muciniphila and its derivatives on cytotoxicity and inflammatory response induced by Clostridioides difficile RT001 in vitro.International microbiology : the official journal of the Spanish Society for Microbiology · 2024Article
- Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Regulation of airway immunity by epithelial miRNAs.Immunological reviews · 2021Review
- Preface to the Proceedings of the 33rd Workshop on Eosinophils in Allergy and Related Diseases 2019 (WEA 2019).Asia Pacific allergy · 2020Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe impaired barrier function of the airway epithelium due to RNA virus infection is closely related to the development and exacerbation of allergic airway inflammation.
objectiveIn this study, we investigated the roles of microRNAs on the mechanisms of double-stranded RNA (dsRNA)-induced epithelial barrier dysfunction.
methods16HBE14o- human bronchial epithelial cells were grown to confluence on Transwell inserts and exposed to poly-I:C. We studied epithelial barrier function by measuring transepithelial electrical resistance and paracellular flux of fluorescent markers and structure of tight junctions by immunofluorescence microscopy.
resultsPoly-I:C treated 16HBE14o- cells increased paracellular permeability. Knockdown of Toll-like receptor 3 and TRIF abrogated these effects. The expression of microRNA-155 (miR-155) was increased by poly-I:C in dose-dependent manner. Transfection of mir155 mimics into 16HBE14o- cells increased permeability and inhibited tight junction formation. Transfection of miR-155 inhibitor suppressed poly-I:C-induced barrier disruption. Poly-I:C treatment significantly decreased the expression of claudin members-claudin-1, -3, -4, -5, -9, -11, -16, -18 and -19. Transfection of miR-155 mimics showed similar changing expression pattern of claudin members with those of poly-I:C treatment.
conclusionThese results suggest that RNA virus infection can impair the epithelial barrier disruption mechanism by down-regulation of claudin members through the induction of miR-155.
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