[gamma]-Secretase Inhibitor Alleviates Acute Airway Inflammation of Allergic Asthma in Mice by Downregulating Th17 Cell Differentiation
T helper 17 (Th17) cells play an important role in the pathogenesis of allergic asthma. Th17 cell differentiation requires Notch signaling. γ-Secretase inhibitor (GSI) blocks Notch signaling; thus, it may be considered as a potential treatment for allergic asthma. The aim of this study was to evalua...
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| Veröffentlicht in: | Mediators of inflammation 2015-01, Vol.2015 |
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| container_title | Mediators of inflammation |
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| creator | Zhang, Weixi Zhang, Xueya Sheng, Anqun Weng, Cuiye Zhu, Tingting Zhao, Wei Li, Changchong |
| description | T helper 17 (Th17) cells play an important role in the pathogenesis of allergic asthma. Th17 cell differentiation requires Notch signaling. γ-Secretase inhibitor (GSI) blocks Notch signaling; thus, it may be considered as a potential treatment for allergic asthma. The aim of this study was to evaluate the effect of GSI on Th17 cell differentiation in a mouse model of allergic asthma. OVA was used to induce mouse asthma model in the presence and absence of GSI. GSI ameliorated the development of OVA-induced asthma, including suppressing airway inflammation responses and reducing the severity of clinical signs. GSI also significantly suppressed Th17-cell responses in spleen and reduced IL-17 levels in serum. These findings suggest that GSI directly regulates Th17 responses through a Notch signaling-dependent pathway in mouse model of allergic asthma, supporting the notion that GSI is a potential therapeutic agent for the treatment of allergic asthma. |
| doi_str_mv | 10.1155/2015/258168 |
| format | Article |
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Th17 cell differentiation requires Notch signaling. γ-Secretase inhibitor (GSI) blocks Notch signaling; thus, it may be considered as a potential treatment for allergic asthma. The aim of this study was to evaluate the effect of GSI on Th17 cell differentiation in a mouse model of allergic asthma. OVA was used to induce mouse asthma model in the presence and absence of GSI. GSI ameliorated the development of OVA-induced asthma, including suppressing airway inflammation responses and reducing the severity of clinical signs. GSI also significantly suppressed Th17-cell responses in spleen and reduced IL-17 levels in serum. These findings suggest that GSI directly regulates Th17 responses through a Notch signaling-dependent pathway in mouse model of allergic asthma, supporting the notion that GSI is a potential therapeutic agent for the treatment of allergic asthma.</description><identifier>ISSN: 0962-9351</identifier><identifier>EISSN: 1466-1861</identifier><identifier>DOI: 10.1155/2015/258168</identifier><language>eng</language><publisher>New York: Hindawi Limited</publisher><subject>Airway management ; Flow cytometry ; Inflammation ; Laboratory animals ; Ligands ; Lymphocytes ; Rodents ; Spleen</subject><ispartof>Mediators of inflammation, 2015-01, Vol.2015</ispartof><rights>Copyright © 2015 Weixi Zhang et al. 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Th17 cell differentiation requires Notch signaling. γ-Secretase inhibitor (GSI) blocks Notch signaling; thus, it may be considered as a potential treatment for allergic asthma. The aim of this study was to evaluate the effect of GSI on Th17 cell differentiation in a mouse model of allergic asthma. OVA was used to induce mouse asthma model in the presence and absence of GSI. GSI ameliorated the development of OVA-induced asthma, including suppressing airway inflammation responses and reducing the severity of clinical signs. GSI also significantly suppressed Th17-cell responses in spleen and reduced IL-17 levels in serum. These findings suggest that GSI directly regulates Th17 responses through a Notch signaling-dependent pathway in mouse model of allergic asthma, supporting the notion that GSI is a potential therapeutic agent for the treatment of allergic asthma.</description><subject>Airway management</subject><subject>Flow cytometry</subject><subject>Inflammation</subject><subject>Laboratory animals</subject><subject>Ligands</subject><subject>Lymphocytes</subject><subject>Rodents</subject><subject>Spleen</subject><issn>0962-9351</issn><issn>1466-1861</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNjk1OwzAUhC0EEuFnxQWexDrg18ZusoxaECxY0R1ClRs9J64cG2yHqifg2piKA7CZWcw3o2HsBvkdohD3M45ZRI2yPmEFVlKWWEs8ZQVv5Kxs5gLP2UWMO865qKq6YN9vvRpH9V6-UhcoqUjw7AazNckHaK2lL6MSRWi7KRG0JuzVIRPa_raS8Q68PnKhNx20MQ2jAuPgxXQE2wOs_N4F6iebYdfDesAFLMlaWBmtKZBL5jhzxc60spGu__yS3T4-rJdP5UfwnxPFtNn5KbgcbXDBm0rk-2L-P-oHvI9X5Q</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Zhang, Weixi</creator><creator>Zhang, Xueya</creator><creator>Sheng, Anqun</creator><creator>Weng, Cuiye</creator><creator>Zhu, Tingting</creator><creator>Zhao, Wei</creator><creator>Li, Changchong</creator><general>Hindawi Limited</general><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope></search><sort><creationdate>20150101</creationdate><title>[gamma]-Secretase Inhibitor Alleviates Acute Airway Inflammation of Allergic Asthma in Mice by Downregulating Th17 Cell Differentiation</title><author>Zhang, Weixi ; Zhang, Xueya ; Sheng, Anqun ; Weng, Cuiye ; Zhu, Tingting ; Zhao, Wei ; Li, Changchong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_17094554453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Airway management</topic><topic>Flow cytometry</topic><topic>Inflammation</topic><topic>Laboratory animals</topic><topic>Ligands</topic><topic>Lymphocytes</topic><topic>Rodents</topic><topic>Spleen</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Weixi</creatorcontrib><creatorcontrib>Zhang, Xueya</creatorcontrib><creatorcontrib>Sheng, Anqun</creatorcontrib><creatorcontrib>Weng, Cuiye</creatorcontrib><creatorcontrib>Zhu, Tingting</creatorcontrib><creatorcontrib>Zhao, Wei</creatorcontrib><creatorcontrib>Li, Changchong</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><jtitle>Mediators of inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Weixi</au><au>Zhang, Xueya</au><au>Sheng, Anqun</au><au>Weng, Cuiye</au><au>Zhu, Tingting</au><au>Zhao, Wei</au><au>Li, Changchong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>[gamma]-Secretase Inhibitor Alleviates Acute Airway Inflammation of Allergic Asthma in Mice by Downregulating Th17 Cell Differentiation</atitle><jtitle>Mediators of inflammation</jtitle><date>2015-01-01</date><risdate>2015</risdate><volume>2015</volume><issn>0962-9351</issn><eissn>1466-1861</eissn><abstract>T helper 17 (Th17) cells play an important role in the pathogenesis of allergic asthma. Th17 cell differentiation requires Notch signaling. γ-Secretase inhibitor (GSI) blocks Notch signaling; thus, it may be considered as a potential treatment for allergic asthma. The aim of this study was to evaluate the effect of GSI on Th17 cell differentiation in a mouse model of allergic asthma. OVA was used to induce mouse asthma model in the presence and absence of GSI. GSI ameliorated the development of OVA-induced asthma, including suppressing airway inflammation responses and reducing the severity of clinical signs. GSI also significantly suppressed Th17-cell responses in spleen and reduced IL-17 levels in serum. These findings suggest that GSI directly regulates Th17 responses through a Notch signaling-dependent pathway in mouse model of allergic asthma, supporting the notion that GSI is a potential therapeutic agent for the treatment of allergic asthma.</abstract><cop>New York</cop><pub>Hindawi Limited</pub><doi>10.1155/2015/258168</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Airway management Flow cytometry Inflammation Laboratory animals Ligands Lymphocytes Rodents Spleen |
| title | [gamma]-Secretase Inhibitor Alleviates Acute Airway Inflammation of Allergic Asthma in Mice by Downregulating Th17 Cell Differentiation |
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