The histone deacetylase inhibitor trichostatin A suppresses murine innate allergic inflammation by blocking group 2 innate lymphoid cell (ILC2) activation
BackgroundGroup 2 innate lymphoid cells (ILC2) are an important source of the type 2 cytokines interleukin (IL)-5 and IL-13 that are critical to the allergic airway phenotype. Previous studies reported that histone deacetylase (HDAC) inhibition by trichostatin A (TSA) downregulated adaptive allergic...
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| Veröffentlicht in: | Thorax 2016-07, Vol.71 (7), p.633-645 |
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| creator | Toki, Shinji Goleniewska, Kasia Reiss, Sara Zhou, Weisong Newcomb, Dawn C Bloodworth, Melissa H Stier, Matthew T Boyd, Kelli L Polosukhin, Vasiliy V Subramaniam, Sriram Peebles, R Stokes |
| description | BackgroundGroup 2 innate lymphoid cells (ILC2) are an important source of the type 2 cytokines interleukin (IL)-5 and IL-13 that are critical to the allergic airway phenotype. Previous studies reported that histone deacetylase (HDAC) inhibition by trichostatin A (TSA) downregulated adaptive allergic immune responses; however, the effect of HDAC inhibition on the early innate allergic immune response is unknown. Therefore, we investigated the effect of TSA on innate airway inflammation mediated by ILC2 activation.MethodsBALB/c mice were challenged intranasally with Alternaria extract, exogenous recombinant mouse IL-33 (rmIL-33) or the respective vehicles for four consecutive days following TSA or vehicle treatment. Bronchoalveolar lavage (BAL) fluids and lungs were harvested 24 h after the last challenge.ResultsWe found that TSA treatment significantly decreased the number of ILC2 expressing IL-5 and IL-13 in the lungs challenged with Alternaria extract or rmIL-33 compared with vehicle treatment (p |
| doi_str_mv | 10.1136/thoraxjnl-2015-207728 |
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Previous studies reported that histone deacetylase (HDAC) inhibition by trichostatin A (TSA) downregulated adaptive allergic immune responses; however, the effect of HDAC inhibition on the early innate allergic immune response is unknown. Therefore, we investigated the effect of TSA on innate airway inflammation mediated by ILC2 activation.MethodsBALB/c mice were challenged intranasally with Alternaria extract, exogenous recombinant mouse IL-33 (rmIL-33) or the respective vehicles for four consecutive days following TSA or vehicle treatment. Bronchoalveolar lavage (BAL) fluids and lungs were harvested 24 h after the last challenge.ResultsWe found that TSA treatment significantly decreased the number of ILC2 expressing IL-5 and IL-13 in the lungs challenged with Alternaria extract or rmIL-33 compared with vehicle treatment (p<0.05). TSA treatment significantly decreased protein expression of IL-5, IL-13, CCL11 and CCL24 in the lung homogenates from Alternaria extract-challenged mice or rmIL-33-challenged mice compared with vehicle treatment (p<0.05). Further, TSA treatment significantly decreased the number of perivascular eosinophils and mucus production in the large airways that are critical components of the asthma phenotype (p<0.05). TSA did not change early IL-33 release in the BAL fluids; however, TSA decreased lung IL-33 expression from epithelial cells 24 h after last Alternaria extract challenge compared with vehicle treatment (p<0.05).ConclusionsThese results reveal that TSA reduces allergen-induced ILC2 activation and the early innate immune responses to an inhaled protease-containing aeroallergen.</description><identifier>ISSN: 0040-6376</identifier><identifier>EISSN: 1468-3296</identifier><identifier>DOI: 10.1136/thoraxjnl-2015-207728</identifier><identifier>PMID: 27071418</identifier><identifier>CODEN: THORA7</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>Allergens - immunology ; Alternaria ; Animals ; Antigens ; Asthma ; Asthma - immunology ; Bronchoalveolar Lavage ; Chemokine CCL11 - metabolism ; Chemokine CCL24 - metabolism ; Cytokines ; Epigenetics ; FDA approval ; Gene expression ; Histone Deacetylase Inhibitors - pharmacology ; Hydroxamic Acids - pharmacology ; Immunity, Innate ; Inflammation ; Interleukin-13 - metabolism ; Interleukin-33 - pharmacology ; Interleukin-5 - metabolism ; Laboratory animals ; Lung - immunology ; Lung diseases ; Lungs ; Lymphocytes - immunology ; Mice ; Mice, Inbred BALB C ; Protein expression ; Proteins ; Respiratory Research ; Vehicles</subject><ispartof>Thorax, 2016-07, Vol.71 (7), p.633-645</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><rights>Copyright: 2016 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/ 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b579t-5e0278adac0d5c9ff3ed6d18889a457c90abe4661ddf92848ce474cd3376393</citedby><cites>FETCH-LOGICAL-b579t-5e0278adac0d5c9ff3ed6d18889a457c90abe4661ddf92848ce474cd3376393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://thorax.bmj.com/content/71/7/633.full.pdf$$EPDF$$P50$$Gbmj$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://thorax.bmj.com/content/71/7/633.full$$EHTML$$P50$$Gbmj$$Hfree_for_read</linktohtml><link.rule.ids>114,115,230,314,776,780,881,3183,23550,27901,27902,77342,77373</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27071418$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Toki, Shinji</creatorcontrib><creatorcontrib>Goleniewska, Kasia</creatorcontrib><creatorcontrib>Reiss, Sara</creatorcontrib><creatorcontrib>Zhou, Weisong</creatorcontrib><creatorcontrib>Newcomb, Dawn C</creatorcontrib><creatorcontrib>Bloodworth, Melissa H</creatorcontrib><creatorcontrib>Stier, Matthew T</creatorcontrib><creatorcontrib>Boyd, Kelli L</creatorcontrib><creatorcontrib>Polosukhin, Vasiliy V</creatorcontrib><creatorcontrib>Subramaniam, Sriram</creatorcontrib><creatorcontrib>Peebles, R Stokes</creatorcontrib><title>The histone deacetylase inhibitor trichostatin A suppresses murine innate allergic inflammation by blocking group 2 innate lymphoid cell (ILC2) activation</title><title>Thorax</title><addtitle>Thorax</addtitle><description>BackgroundGroup 2 innate lymphoid cells (ILC2) are an important source of the type 2 cytokines interleukin (IL)-5 and IL-13 that are critical to the allergic airway phenotype. Previous studies reported that histone deacetylase (HDAC) inhibition by trichostatin A (TSA) downregulated adaptive allergic immune responses; however, the effect of HDAC inhibition on the early innate allergic immune response is unknown. Therefore, we investigated the effect of TSA on innate airway inflammation mediated by ILC2 activation.MethodsBALB/c mice were challenged intranasally with Alternaria extract, exogenous recombinant mouse IL-33 (rmIL-33) or the respective vehicles for four consecutive days following TSA or vehicle treatment. Bronchoalveolar lavage (BAL) fluids and lungs were harvested 24 h after the last challenge.ResultsWe found that TSA treatment significantly decreased the number of ILC2 expressing IL-5 and IL-13 in the lungs challenged with Alternaria extract or rmIL-33 compared with vehicle treatment (p<0.05). TSA treatment significantly decreased protein expression of IL-5, IL-13, CCL11 and CCL24 in the lung homogenates from Alternaria extract-challenged mice or rmIL-33-challenged mice compared with vehicle treatment (p<0.05). Further, TSA treatment significantly decreased the number of perivascular eosinophils and mucus production in the large airways that are critical components of the asthma phenotype (p<0.05). TSA did not change early IL-33 release in the BAL fluids; however, TSA decreased lung IL-33 expression from epithelial cells 24 h after last Alternaria extract challenge compared with vehicle treatment (p<0.05).ConclusionsThese results reveal that TSA reduces allergen-induced ILC2 activation and the early innate immune responses to an inhaled protease-containing aeroallergen.</description><subject>Allergens - immunology</subject><subject>Alternaria</subject><subject>Animals</subject><subject>Antigens</subject><subject>Asthma</subject><subject>Asthma - immunology</subject><subject>Bronchoalveolar Lavage</subject><subject>Chemokine CCL11 - metabolism</subject><subject>Chemokine CCL24 - metabolism</subject><subject>Cytokines</subject><subject>Epigenetics</subject><subject>FDA approval</subject><subject>Gene expression</subject><subject>Histone Deacetylase Inhibitors - pharmacology</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Immunity, Innate</subject><subject>Inflammation</subject><subject>Interleukin-13 - metabolism</subject><subject>Interleukin-33 - pharmacology</subject><subject>Interleukin-5 - metabolism</subject><subject>Laboratory animals</subject><subject>Lung - immunology</subject><subject>Lung diseases</subject><subject>Lungs</subject><subject>Lymphocytes - immunology</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Respiratory Research</subject><subject>Vehicles</subject><issn>0040-6376</issn><issn>1468-3296</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>9YT</sourceid><sourceid>ACMMV</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNksFu1DAQhi0EokvhEUCWuJRDwHbs2L4gVSsolVbiQO-W4zgbL44dbKfqvgpPS7bbroALXMYa-ft_zYx-AF5j9B7juvlQhpj03S74iiDMlsI5EU_ACtNGVDWRzVOwQoiiqql5cwZe5LxDCAmM-XNwRjjimGKxAj9vBgsHl0sMFnZWG1v2XmcLXRhc60pMsCRnhpiLLi7AS5jnaUo2Z5vhOCcXDmjQxULtvU1bZ5a-93ocFz4G2O5h66P57sIWblOcJ0geBX4_TkN0HTTWe3hxvVmTd1Cb4m7vpS_Bs177bF89vOfg2-dPN-sv1ebr1fX6clO1jMtSMYsIF7rTBnXMyL6vbdd0WAghNWXcSKRbS5sGd10viaDCWMqp6erlLrWsz8HHo-s0t6PtjA0laa-m5Ead9ipqp_78CW5Q23irqKQYi4PBxYNBij9mm4saXT5spIONc1ZY1IQwxAj7N8olZ7RmFC3o27_QXZxTWO6wGCJMBaMSLxQ7UibFnJPtT3NjpA4xUaeYqENM1DEmi-7N70ufVI-5WAB0BNpx95-evwAmPc76</recordid><startdate>20160701</startdate><enddate>20160701</enddate><creator>Toki, Shinji</creator><creator>Goleniewska, Kasia</creator><creator>Reiss, Sara</creator><creator>Zhou, Weisong</creator><creator>Newcomb, Dawn C</creator><creator>Bloodworth, Melissa H</creator><creator>Stier, Matthew T</creator><creator>Boyd, Kelli L</creator><creator>Polosukhin, Vasiliy V</creator><creator>Subramaniam, Sriram</creator><creator>Peebles, R Stokes</creator><general>BMJ Publishing Group LTD</general><general>BMJ Publishing Group</general><scope>9YT</scope><scope>ACMMV</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20160701</creationdate><title>The histone deacetylase inhibitor trichostatin A suppresses murine innate allergic inflammation by blocking group 2 innate lymphoid cell (ILC2) activation</title><author>Toki, Shinji ; Goleniewska, Kasia ; Reiss, Sara ; Zhou, Weisong ; Newcomb, Dawn C ; Bloodworth, Melissa H ; Stier, Matthew T ; Boyd, Kelli L ; Polosukhin, Vasiliy V ; Subramaniam, Sriram ; Peebles, R Stokes</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b579t-5e0278adac0d5c9ff3ed6d18889a457c90abe4661ddf92848ce474cd3376393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Allergens - immunology</topic><topic>Alternaria</topic><topic>Animals</topic><topic>Antigens</topic><topic>Asthma</topic><topic>Asthma - immunology</topic><topic>Bronchoalveolar Lavage</topic><topic>Chemokine CCL11 - metabolism</topic><topic>Chemokine CCL24 - metabolism</topic><topic>Cytokines</topic><topic>Epigenetics</topic><topic>FDA approval</topic><topic>Gene expression</topic><topic>Histone Deacetylase Inhibitors - pharmacology</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Immunity, Innate</topic><topic>Inflammation</topic><topic>Interleukin-13 - metabolism</topic><topic>Interleukin-33 - pharmacology</topic><topic>Interleukin-5 - metabolism</topic><topic>Laboratory animals</topic><topic>Lung - immunology</topic><topic>Lung diseases</topic><topic>Lungs</topic><topic>Lymphocytes - immunology</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Respiratory Research</topic><topic>Vehicles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Toki, Shinji</creatorcontrib><creatorcontrib>Goleniewska, Kasia</creatorcontrib><creatorcontrib>Reiss, Sara</creatorcontrib><creatorcontrib>Zhou, Weisong</creatorcontrib><creatorcontrib>Newcomb, Dawn C</creatorcontrib><creatorcontrib>Bloodworth, Melissa H</creatorcontrib><creatorcontrib>Stier, Matthew T</creatorcontrib><creatorcontrib>Boyd, Kelli L</creatorcontrib><creatorcontrib>Polosukhin, Vasiliy V</creatorcontrib><creatorcontrib>Subramaniam, Sriram</creatorcontrib><creatorcontrib>Peebles, R Stokes</creatorcontrib><collection>BMJ Open Access Journals</collection><collection>BMJ Journals:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Thorax</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Toki, Shinji</au><au>Goleniewska, Kasia</au><au>Reiss, Sara</au><au>Zhou, Weisong</au><au>Newcomb, Dawn C</au><au>Bloodworth, Melissa H</au><au>Stier, Matthew T</au><au>Boyd, Kelli L</au><au>Polosukhin, Vasiliy V</au><au>Subramaniam, Sriram</au><au>Peebles, R Stokes</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The histone deacetylase inhibitor trichostatin A suppresses murine innate allergic inflammation by blocking group 2 innate lymphoid cell (ILC2) activation</atitle><jtitle>Thorax</jtitle><addtitle>Thorax</addtitle><date>2016-07-01</date><risdate>2016</risdate><volume>71</volume><issue>7</issue><spage>633</spage><epage>645</epage><pages>633-645</pages><issn>0040-6376</issn><eissn>1468-3296</eissn><coden>THORA7</coden><abstract>BackgroundGroup 2 innate lymphoid cells (ILC2) are an important source of the type 2 cytokines interleukin (IL)-5 and IL-13 that are critical to the allergic airway phenotype. Previous studies reported that histone deacetylase (HDAC) inhibition by trichostatin A (TSA) downregulated adaptive allergic immune responses; however, the effect of HDAC inhibition on the early innate allergic immune response is unknown. Therefore, we investigated the effect of TSA on innate airway inflammation mediated by ILC2 activation.MethodsBALB/c mice were challenged intranasally with Alternaria extract, exogenous recombinant mouse IL-33 (rmIL-33) or the respective vehicles for four consecutive days following TSA or vehicle treatment. Bronchoalveolar lavage (BAL) fluids and lungs were harvested 24 h after the last challenge.ResultsWe found that TSA treatment significantly decreased the number of ILC2 expressing IL-5 and IL-13 in the lungs challenged with Alternaria extract or rmIL-33 compared with vehicle treatment (p<0.05). TSA treatment significantly decreased protein expression of IL-5, IL-13, CCL11 and CCL24 in the lung homogenates from Alternaria extract-challenged mice or rmIL-33-challenged mice compared with vehicle treatment (p<0.05). Further, TSA treatment significantly decreased the number of perivascular eosinophils and mucus production in the large airways that are critical components of the asthma phenotype (p<0.05). TSA did not change early IL-33 release in the BAL fluids; however, TSA decreased lung IL-33 expression from epithelial cells 24 h after last Alternaria extract challenge compared with vehicle treatment (p<0.05).ConclusionsThese results reveal that TSA reduces allergen-induced ILC2 activation and the early innate immune responses to an inhaled protease-containing aeroallergen.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>27071418</pmid><doi>10.1136/thoraxjnl-2015-207728</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Allergens - immunology Alternaria Animals Antigens Asthma Asthma - immunology Bronchoalveolar Lavage Chemokine CCL11 - metabolism Chemokine CCL24 - metabolism Cytokines Epigenetics FDA approval Gene expression Histone Deacetylase Inhibitors - pharmacology Hydroxamic Acids - pharmacology Immunity, Innate Inflammation Interleukin-13 - metabolism Interleukin-33 - pharmacology Interleukin-5 - metabolism Laboratory animals Lung - immunology Lung diseases Lungs Lymphocytes - immunology Mice Mice, Inbred BALB C Protein expression Proteins Respiratory Research Vehicles |
| title | The histone deacetylase inhibitor trichostatin A suppresses murine innate allergic inflammation by blocking group 2 innate lymphoid cell (ILC2) activation |
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