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DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins

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)-indu...

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Autores principales: Hiranuma, Hisato, Gon, Yasuhiro, Maruoka, Shuichiro, Kozu, Yutaka, Yamada, Shiho, Fukuda, Asami, Kurosawa, Yusuke, Tetsuo, Shimizu, Nakagawa, Yoshiko, Mizumura, Kenji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Asia Pacific Association of Allergy, Asthma and Clinical Immunology 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7203438/
https://www.ncbi.nlm.nih.gov/pubmed/32411585
http://dx.doi.org/10.5415/apallergy.2020.10.e20
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author Hiranuma, Hisato
Gon, Yasuhiro
Maruoka, Shuichiro
Kozu, Yutaka
Yamada, Shiho
Fukuda, Asami
Kurosawa, Yusuke
Tetsuo, Shimizu
Nakagawa, Yoshiko
Mizumura, Kenji
author_facet Hiranuma, Hisato
Gon, Yasuhiro
Maruoka, Shuichiro
Kozu, Yutaka
Yamada, Shiho
Fukuda, Asami
Kurosawa, Yusuke
Tetsuo, Shimizu
Nakagawa, Yoshiko
Mizumura, Kenji
author_sort Hiranuma, Hisato
collection PubMed
description 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-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. RESULTS: Poly-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. 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.
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spelling pubmed-72034382020-05-14 DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins Hiranuma, Hisato Gon, Yasuhiro Maruoka, Shuichiro Kozu, Yutaka Yamada, Shiho Fukuda, Asami Kurosawa, Yusuke Tetsuo, Shimizu Nakagawa, Yoshiko Mizumura, Kenji Asia Pac Allergy Original Article 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-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. RESULTS: Poly-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. 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. Asia Pacific Association of Allergy, Asthma and Clinical Immunology 2020-04-27 /pmc/articles/PMC7203438/ /pubmed/32411585 http://dx.doi.org/10.5415/apallergy.2020.10.e20 Text en Copyright © 2020. Asia Pacific Association of Allergy, Asthma and Clinical Immunology. https://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Hiranuma, Hisato
Gon, Yasuhiro
Maruoka, Shuichiro
Kozu, Yutaka
Yamada, Shiho
Fukuda, Asami
Kurosawa, Yusuke
Tetsuo, Shimizu
Nakagawa, Yoshiko
Mizumura, Kenji
DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins
title DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins
title_full DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins
title_fullStr DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins
title_full_unstemmed DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins
title_short DsRNA induction of microRNA-155 disrupt tight junction barrier by modulating claudins
title_sort dsrna induction of microrna-155 disrupt tight junction barrier by modulating claudins
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7203438/
https://www.ncbi.nlm.nih.gov/pubmed/32411585
http://dx.doi.org/10.5415/apallergy.2020.10.e20
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