Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo

Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV r...
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Autor*in:	Fuming Zhang [verfasserIn] Xiaofang Sun [verfasserIn] Ya Zhu [verfasserIn] Wangsen Qin [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	miR-146a Influenza A virus TRAF6 Type I IFN response

Übergeordnetes Werk:	In: Biomedicine & Pharmacotherapy - Elsevier, 2021, 111(2019), Seite 740-750
Übergeordnetes Werk:	volume:111 ; year:2019 ; pages:740-750

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.biopha.2018.12.103

Katalog-ID:	DOAJ002301253

Internformat


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520			\|a Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection.
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Indexfelder

author_variant	f z fz x s xs y z yz w q wq
matchkey_str	article:19506007:2019----::oneuainfi16ihbtifunavrselctobehnightpine
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publishDate	2019
allfields	10.1016/j.biopha.2018.12.103 doi (DE-627)DOAJ002301253 (DE-599)DOAJ5b8357dc208d4311b3302cc7b71ba70b DE-627 ger DE-627 rakwb eng RM1-950 Fuming Zhang verfasserin aut Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection. miR-146a Influenza A virus TRAF6 Type I IFN response Therapeutics. Pharmacology Xiaofang Sun verfasserin aut Ya Zhu verfasserin aut Wangsen Qin verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 111(2019), Seite 740-750 (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:111 year:2019 pages:740-750 https://doi.org/10.1016/j.biopha.2018.12.103 kostenfrei https://doaj.org/article/5b8357dc208d4311b3302cc7b71ba70b kostenfrei http://www.sciencedirect.com/science/article/pii/S075333221834616X kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 111 2019 740-750
spelling	10.1016/j.biopha.2018.12.103 doi (DE-627)DOAJ002301253 (DE-599)DOAJ5b8357dc208d4311b3302cc7b71ba70b DE-627 ger DE-627 rakwb eng RM1-950 Fuming Zhang verfasserin aut Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection. miR-146a Influenza A virus TRAF6 Type I IFN response Therapeutics. Pharmacology Xiaofang Sun verfasserin aut Ya Zhu verfasserin aut Wangsen Qin verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 111(2019), Seite 740-750 (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:111 year:2019 pages:740-750 https://doi.org/10.1016/j.biopha.2018.12.103 kostenfrei https://doaj.org/article/5b8357dc208d4311b3302cc7b71ba70b kostenfrei http://www.sciencedirect.com/science/article/pii/S075333221834616X kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 111 2019 740-750
allfields_unstemmed	10.1016/j.biopha.2018.12.103 doi (DE-627)DOAJ002301253 (DE-599)DOAJ5b8357dc208d4311b3302cc7b71ba70b DE-627 ger DE-627 rakwb eng RM1-950 Fuming Zhang verfasserin aut Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection. miR-146a Influenza A virus TRAF6 Type I IFN response Therapeutics. Pharmacology Xiaofang Sun verfasserin aut Ya Zhu verfasserin aut Wangsen Qin verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 111(2019), Seite 740-750 (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:111 year:2019 pages:740-750 https://doi.org/10.1016/j.biopha.2018.12.103 kostenfrei https://doaj.org/article/5b8357dc208d4311b3302cc7b71ba70b kostenfrei http://www.sciencedirect.com/science/article/pii/S075333221834616X kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 111 2019 740-750
allfieldsGer	10.1016/j.biopha.2018.12.103 doi (DE-627)DOAJ002301253 (DE-599)DOAJ5b8357dc208d4311b3302cc7b71ba70b DE-627 ger DE-627 rakwb eng RM1-950 Fuming Zhang verfasserin aut Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection. miR-146a Influenza A virus TRAF6 Type I IFN response Therapeutics. Pharmacology Xiaofang Sun verfasserin aut Ya Zhu verfasserin aut Wangsen Qin verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 111(2019), Seite 740-750 (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:111 year:2019 pages:740-750 https://doi.org/10.1016/j.biopha.2018.12.103 kostenfrei https://doaj.org/article/5b8357dc208d4311b3302cc7b71ba70b kostenfrei http://www.sciencedirect.com/science/article/pii/S075333221834616X kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 111 2019 740-750
allfieldsSound	10.1016/j.biopha.2018.12.103 doi (DE-627)DOAJ002301253 (DE-599)DOAJ5b8357dc208d4311b3302cc7b71ba70b DE-627 ger DE-627 rakwb eng RM1-950 Fuming Zhang verfasserin aut Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection. miR-146a Influenza A virus TRAF6 Type I IFN response Therapeutics. Pharmacology Xiaofang Sun verfasserin aut Ya Zhu verfasserin aut Wangsen Qin verfasserin aut In Biomedicine & Pharmacotherapy Elsevier, 2021 111(2019), Seite 740-750 (DE-627)306717565 (DE-600)1501510-5 19506007 nnns volume:111 year:2019 pages:740-750 https://doi.org/10.1016/j.biopha.2018.12.103 kostenfrei https://doaj.org/article/5b8357dc208d4311b3302cc7b71ba70b kostenfrei http://www.sciencedirect.com/science/article/pii/S075333221834616X kostenfrei https://doaj.org/toc/0753-3322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 111 2019 740-750
language	English
source	In Biomedicine & Pharmacotherapy 111(2019), Seite 740-750 volume:111 year:2019 pages:740-750
sourceStr	In Biomedicine & Pharmacotherapy 111(2019), Seite 740-750 volume:111 year:2019 pages:740-750
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	miR-146a Influenza A virus TRAF6 Type I IFN response Therapeutics. Pharmacology
isfreeaccess_bool	true
container_title	Biomedicine & Pharmacotherapy
authorswithroles_txt_mv	Fuming Zhang @@aut@@ Xiaofang Sun @@aut@@ Ya Zhu @@aut@@ Wangsen Qin @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	306717565
id	DOAJ002301253
language_de	englisch
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callnumber-first	R - Medicine
author	Fuming Zhang
spellingShingle	Fuming Zhang misc RM1-950 misc miR-146a misc Influenza A virus misc TRAF6 misc Type I IFN response misc Therapeutics. Pharmacology Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo
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topic_title	RM1-950 Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo miR-146a Influenza A virus TRAF6 Type I IFN response
topic	misc RM1-950 misc miR-146a misc Influenza A virus misc TRAF6 misc Type I IFN response misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc miR-146a misc Influenza A virus misc TRAF6 misc Type I IFN response misc Therapeutics. Pharmacology
topic_browse	misc RM1-950 misc miR-146a misc Influenza A virus misc TRAF6 misc Type I IFN response misc Therapeutics. Pharmacology
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title	Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo
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title_full	Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo
author_sort	Fuming Zhang
journal	Biomedicine & Pharmacotherapy
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author_browse	Fuming Zhang Xiaofang Sun Ya Zhu Wangsen Qin
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title_sort	downregulation of mir-146a inhibits influenza a virus replication by enhancing the type i interferon response in vitro and in vivo
callnumber	RM1-950
title_auth	Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo
abstract	Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection.
abstractGer	Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection.
abstract_unstemmed	Albeit microRNAs (miRNAs) have become increasingly appreciated for their essential roles in innate immune responses to viral infections; however, it is unknown how host miRNAs regulate influenza A virus (IAV)-induced inflammation. The aim of our study was to investigate the role of miR-146a in IAV replication in vitro and in vivo. In vitro, we found miR-146a was significantly upregulated in A549 cells with IAV infection. Overexpression of miR-146a promoted IAV replication, while downregulation of miR-146a repressed replication. We found that miR-146a diminished type I interferon (IFN) responses by decreasing IFN-β production and IFN-stimulated gene (ISG) expression. Furthermore, we found the IFNs level and IAV replication regulated by miR-146a inhibitor was partially reversed by depletion of interferon receptor (IFNAR) 1 or 2. In addition, we found that miR-146a directly targets tumor necrosis factor receptor association factor 6 (TRAF6), which is involved in the production of type I IFN, and TRAF6 overexpression reversed the replication-promoting effect of miR-146a on IAV. In vivo, inhibition of miR-146a alleviated IAV-induced mice lung injury and promoted survival rates by promoting type I antiviral activities. It is, therefore, concluded that downregulation of miR-146a inhibits IAV replication by enhancing type I IFN response through its target gene TRAF6 in vitro and in vivo, suggesting miR-146a antagomir might be a potential therapeutic target during IAV infection.
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title_short	Downregulation of miR-146a inhibits influenza A virus replication by enhancing the type I interferon response in vitro and in vivo
url	https://doi.org/10.1016/j.biopha.2018.12.103 https://doaj.org/article/5b8357dc208d4311b3302cc7b71ba70b http://www.sciencedirect.com/science/article/pii/S075333221834616X https://doaj.org/toc/0753-3322
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up_date	2024-07-04T00:41:23.075Z
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