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IL-17F Induces CCL20 in Bronchial Epithelial Cells

IL-17F plays a crucial role in airway inflammatory diseases including asthma, but its function has not been fully elucidated. CCL20 is also involved in allergic airway inflammation, while its regulatory mechanisms remain to be defined. To further identify a novel role of IL-17F, the expression of CC...

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Autores principales: Nozato, Kyoko, Fujita, Junichi, Kawaguchi, Mio, Ohara, Gen, Morishima, Yuko, Ishii, Yukio, Huang, Shau-Ku, Kokubu, Fumio, Satoh, Hiroaki, Hizawa, Nobuyuki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195431/
https://www.ncbi.nlm.nih.gov/pubmed/22013453
http://dx.doi.org/10.1155/2011/587204
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author Nozato, Kyoko
Fujita, Junichi
Kawaguchi, Mio
Ohara, Gen
Morishima, Yuko
Ishii, Yukio
Huang, Shau-Ku
Kokubu, Fumio
Satoh, Hiroaki
Hizawa, Nobuyuki
author_facet Nozato, Kyoko
Fujita, Junichi
Kawaguchi, Mio
Ohara, Gen
Morishima, Yuko
Ishii, Yukio
Huang, Shau-Ku
Kokubu, Fumio
Satoh, Hiroaki
Hizawa, Nobuyuki
author_sort Nozato, Kyoko
collection PubMed
description IL-17F plays a crucial role in airway inflammatory diseases including asthma, but its function has not been fully elucidated. CCL20 is also involved in allergic airway inflammation, while its regulatory mechanisms remain to be defined. To further identify a novel role of IL-17F, the expression of CCL20 by IL-17F in bronchial epithelial cells and the signaling mechanisms involved were investigated. Bronchial epithelial cells were stimulated with IL-17F, and the levels of CCL20 gene and protein measured, with the effects of the addition of various kinase inhibitors and siRNAs also investigated. IL-17F significantly induced the expression of CCL20 gene and protein. Pretreatment with inhibitors for MEK1/2, Raf1 and MSK1, and overexpression of a Raf1 dominant-negative mutant significantly diminished IL-17F-induced CCL20 production. Moreover, transfection of the siRNAs targeting MSK1, p90RSK, and CREB blocked CCL20 expression. These findings suggest that IL-17F is able to induce CCL20 via Raf1-MEK1/2-ERK1/2-MSK1/p90RSK-CREB signaling pathway in bronchial epithelial cells. The IL-17F/CCL20 axis may be a novel pharmacological target for asthma.
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spelling pubmed-31954312011-10-19 IL-17F Induces CCL20 in Bronchial Epithelial Cells Nozato, Kyoko Fujita, Junichi Kawaguchi, Mio Ohara, Gen Morishima, Yuko Ishii, Yukio Huang, Shau-Ku Kokubu, Fumio Satoh, Hiroaki Hizawa, Nobuyuki J Allergy (Cairo) Research Article IL-17F plays a crucial role in airway inflammatory diseases including asthma, but its function has not been fully elucidated. CCL20 is also involved in allergic airway inflammation, while its regulatory mechanisms remain to be defined. To further identify a novel role of IL-17F, the expression of CCL20 by IL-17F in bronchial epithelial cells and the signaling mechanisms involved were investigated. Bronchial epithelial cells were stimulated with IL-17F, and the levels of CCL20 gene and protein measured, with the effects of the addition of various kinase inhibitors and siRNAs also investigated. IL-17F significantly induced the expression of CCL20 gene and protein. Pretreatment with inhibitors for MEK1/2, Raf1 and MSK1, and overexpression of a Raf1 dominant-negative mutant significantly diminished IL-17F-induced CCL20 production. Moreover, transfection of the siRNAs targeting MSK1, p90RSK, and CREB blocked CCL20 expression. These findings suggest that IL-17F is able to induce CCL20 via Raf1-MEK1/2-ERK1/2-MSK1/p90RSK-CREB signaling pathway in bronchial epithelial cells. The IL-17F/CCL20 axis may be a novel pharmacological target for asthma. Hindawi Publishing Corporation 2011 2011-10-13 /pmc/articles/PMC3195431/ /pubmed/22013453 http://dx.doi.org/10.1155/2011/587204 Text en Copyright © 2011 Kyoko Nozato et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Nozato, Kyoko
Fujita, Junichi
Kawaguchi, Mio
Ohara, Gen
Morishima, Yuko
Ishii, Yukio
Huang, Shau-Ku
Kokubu, Fumio
Satoh, Hiroaki
Hizawa, Nobuyuki
IL-17F Induces CCL20 in Bronchial Epithelial Cells
title IL-17F Induces CCL20 in Bronchial Epithelial Cells
title_full IL-17F Induces CCL20 in Bronchial Epithelial Cells
title_fullStr IL-17F Induces CCL20 in Bronchial Epithelial Cells
title_full_unstemmed IL-17F Induces CCL20 in Bronchial Epithelial Cells
title_short IL-17F Induces CCL20 in Bronchial Epithelial Cells
title_sort il-17f induces ccl20 in bronchial epithelial cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195431/
https://www.ncbi.nlm.nih.gov/pubmed/22013453
http://dx.doi.org/10.1155/2011/587204
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