國家衛生研究院 NHRI:Item 3990099045/10590

NHRI > National Institute of Environmental Health Sciences > Shau-Ku Huang > Conference Papers/Meeting Abstract > Item 3990099045/10590

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/10590

Title:	Il-17f induces Il-6 Via tak1-Nf kappaB pathway in airway smooth muscle cells
Other Titles:	Il-17f induces Il-6 Via tak1-Nf κB pathway in airway smooth muscle cells
Authors:	Nakajima, M;Kawaguchi, M;Ota, K;Fujita, J;Matsukura, S;Huang, SK;Masuko, H;Kiwamoto, T;Matsuno, Y;Morishima, Y;Ishii, Y;Satoh, H;Sakamoto, T;Hizawa, N
Contributors:	National Institute of Environmental Health Sciences
Abstract:	Airway smooth muscle (ASM) cells are thought to contribute to the pathogenesis of allergic asthma by orchestrating and perpetuating airway inflammation and remodeling responses. In this study, we evaluated the IL-17RA signal transduction and gene expression profile in ASM cells from subjects with mild asthma and healthy individuals. Human primary ASM cells were treated with IL-17A and probed by the Affymetrix GeneChip array, and gene targets were validated by real-time quantitative RT-PCR. Genomic analysis underlined the proinflammatory nature of IL-17A, as multiple NF-κB regulatory factors and chemokines were induced in ASM cells. Transcriptional regulators consisting of primary response genes were overrepresented and displayed dynamic expression profiles. IL-17A poorly enhanced IL-1β or IL-22 gene responses in ASM cells from both subjects with mild asthma and healthy donors. Interestingly, protein modifications to the NF-κB regulatory network were not observed after IL-17A stimulation, although oscillations in IκBε expression were detected. ASM cells from subjects with mild asthma up-regulated more genes with greater overall variability in response to IL-17A than from healthy donors. Finally, in response to IL-17A, ASM cells displayed rapid activation of the extracellular signal–regulated kinase/ribosomal S6 kinase signaling pathway and increased nuclear levels of phosphorylated extracellular signal–regulated kinase. Taken together, our results suggest that IL-17A mediated modest gene expression response, which, in cooperation with the NF-κB signaling network, may regulate the gene expression profile in ASM cells.
Date:	2017-05
Relation:	American Journal of Respiratory and Critical Care Medicine. 2017 May;195:A5302.
Link to:	http://www.atsjournals.org/doi/pdf/10.1164/ajrccm-conference.2017.195.1_MeetingAbstracts.A5302
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1073-449X&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000400372505105
Appears in Collections:	[Shau-Ku Huang] Conference Papers/Meeting Abstract

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