DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins.
Asia Pac Allergy
; 10(2): e20, 2020 Apr.
Article
em En
| MEDLINE
| ID: mdl-32411585
ABSTRACT
BACKGROUND:
The impaired barrier function of the airway epithelium due to RNA virus infection is closely related to the development and exacerbation of allergic airway inflammation.OBJECTIVE:
In this study, we investigated the roles of microRNAs on the mechanisms of double-stranded RNA (dsRNA)-induced epithelial barrier dysfunction.METHODS:
16HBE14o- human bronchial epithelial cells were grown to confluence on Transwell inserts and exposed to poly-IC. We studied epithelial barrier function by measuring transepithelial electrical resistance and paracellular flux of fluorescent markers and structure of tight junctions by immunofluorescence microscopy.RESULTS:
Poly-IC 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-IC 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-IC-induced barrier disruption. Poly-IC 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-IC treatment.CONCLUSION:
These 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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Asia Pac Allergy
Ano de publicação:
2020
Tipo de documento:
Article
País de afiliação:
Japão