Fstl1 Promotes Asthmatic Airway Remodeling by Inducing Oncostatin M
Chronic asthma is associated with airway remodeling and decline in lung function. In this article, we show that follistatin-like 1 (Fstl1), a mediator not previously associated with asthma, is highly expressed by macrophages in the lungs of humans with severe asthma. Chronic allergen-challenged Lys-...
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| Veröffentlicht in: | The Journal of immunology (1950) 2015-10, Vol.195 (8), p.3546-3556 |
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| creator | Miller, Marina Beppu, Andrew Rosenthal, Peter Pham, Alexa Das, Sudipta Karta, Maya Song, Dae Jin Vuong, Christine Doherty, Taylor Croft, Michael Zuraw, Bruce Zhang, Xu Gao, Xiang Aceves, Seema Chouiali, Fazila Hamid, Qutayba Broide, David H |
| description | Chronic asthma is associated with airway remodeling and decline in lung function. In this article, we show that follistatin-like 1 (Fstl1), a mediator not previously associated with asthma, is highly expressed by macrophages in the lungs of humans with severe asthma. Chronic allergen-challenged Lys-Cre(tg) /Fstl1(Δ/Δ) mice in whom Fstl1 is inactivated in macrophages/myeloid cells had significantly reduced airway remodeling and reduced levels of oncostatin M (OSM), a cytokine previously not known to be regulated by Fstl1. The importance of the Fstl1 induction of OSM to airway remodeling was demonstrated in murine studies in which administration of Fstl1 induced airway remodeling and increased OSM, whereas administration of an anti-OSM Ab blocked the effect of Fstl1 on inducing airway remodeling, eosinophilic airway inflammation, and airway hyperresponsiveness, all cardinal features of asthma. Overall, these studies demonstrate that the Fstl1/OSM pathway may be a novel pathway to inhibit airway remodeling in severe human asthma. |
| doi_str_mv | 10.4049/jimmunol.1501105 |
| format | Article |
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In this article, we show that follistatin-like 1 (Fstl1), a mediator not previously associated with asthma, is highly expressed by macrophages in the lungs of humans with severe asthma. Chronic allergen-challenged Lys-Cre(tg) /Fstl1(Δ/Δ) mice in whom Fstl1 is inactivated in macrophages/myeloid cells had significantly reduced airway remodeling and reduced levels of oncostatin M (OSM), a cytokine previously not known to be regulated by Fstl1. The importance of the Fstl1 induction of OSM to airway remodeling was demonstrated in murine studies in which administration of Fstl1 induced airway remodeling and increased OSM, whereas administration of an anti-OSM Ab blocked the effect of Fstl1 on inducing airway remodeling, eosinophilic airway inflammation, and airway hyperresponsiveness, all cardinal features of asthma. Overall, these studies demonstrate that the Fstl1/OSM pathway may be a novel pathway to inhibit airway remodeling in severe human asthma.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1501105</identifier><identifier>PMID: 26355153</identifier><language>eng</language><publisher>United States</publisher><subject>Airway Remodeling - drug effects ; Airway Remodeling - genetics ; Airway Remodeling - immunology ; Animals ; Antibodies - immunology ; Antibodies - pharmacology ; Asthma - genetics ; Asthma - immunology ; Asthma - pathology ; Female ; Follistatin-Related Proteins - genetics ; Follistatin-Related Proteins - immunology ; Humans ; Macrophages - immunology ; Macrophages - pathology ; Male ; Mice ; Oncostatin M - genetics ; Oncostatin M - immunology ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Signal Transduction - immunology</subject><ispartof>The Journal of immunology (1950), 2015-10, Vol.195 (8), p.3546-3556</ispartof><rights>Copyright © 2015 by The American Association of Immunologists, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-3ed6e6d65edb952dedae135bd9a374e16dffe2307525c2868c1995ca97275b943</citedby><cites>FETCH-LOGICAL-c495t-3ed6e6d65edb952dedae135bd9a374e16dffe2307525c2868c1995ca97275b943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26355153$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miller, Marina</creatorcontrib><creatorcontrib>Beppu, Andrew</creatorcontrib><creatorcontrib>Rosenthal, Peter</creatorcontrib><creatorcontrib>Pham, Alexa</creatorcontrib><creatorcontrib>Das, Sudipta</creatorcontrib><creatorcontrib>Karta, Maya</creatorcontrib><creatorcontrib>Song, Dae Jin</creatorcontrib><creatorcontrib>Vuong, Christine</creatorcontrib><creatorcontrib>Doherty, Taylor</creatorcontrib><creatorcontrib>Croft, Michael</creatorcontrib><creatorcontrib>Zuraw, Bruce</creatorcontrib><creatorcontrib>Zhang, Xu</creatorcontrib><creatorcontrib>Gao, Xiang</creatorcontrib><creatorcontrib>Aceves, Seema</creatorcontrib><creatorcontrib>Chouiali, Fazila</creatorcontrib><creatorcontrib>Hamid, Qutayba</creatorcontrib><creatorcontrib>Broide, David H</creatorcontrib><title>Fstl1 Promotes Asthmatic Airway Remodeling by Inducing Oncostatin M</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Chronic asthma is associated with airway remodeling and decline in lung function. In this article, we show that follistatin-like 1 (Fstl1), a mediator not previously associated with asthma, is highly expressed by macrophages in the lungs of humans with severe asthma. Chronic allergen-challenged Lys-Cre(tg) /Fstl1(Δ/Δ) mice in whom Fstl1 is inactivated in macrophages/myeloid cells had significantly reduced airway remodeling and reduced levels of oncostatin M (OSM), a cytokine previously not known to be regulated by Fstl1. The importance of the Fstl1 induction of OSM to airway remodeling was demonstrated in murine studies in which administration of Fstl1 induced airway remodeling and increased OSM, whereas administration of an anti-OSM Ab blocked the effect of Fstl1 on inducing airway remodeling, eosinophilic airway inflammation, and airway hyperresponsiveness, all cardinal features of asthma. Overall, these studies demonstrate that the Fstl1/OSM pathway may be a novel pathway to inhibit airway remodeling in severe human asthma.</description><subject>Airway Remodeling - drug effects</subject><subject>Airway Remodeling - genetics</subject><subject>Airway Remodeling - immunology</subject><subject>Animals</subject><subject>Antibodies - immunology</subject><subject>Antibodies - pharmacology</subject><subject>Asthma - genetics</subject><subject>Asthma - immunology</subject><subject>Asthma - pathology</subject><subject>Female</subject><subject>Follistatin-Related Proteins - genetics</subject><subject>Follistatin-Related Proteins - immunology</subject><subject>Humans</subject><subject>Macrophages - immunology</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Oncostatin M - genetics</subject><subject>Oncostatin M - immunology</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - immunology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1P20AQhldVUQmBe0-Vj72Yzuyn91IpigpEAoFQe16tdyfByPZSr02Vf08iAmpPPc1I88yrGT2MfUY4lyDtt8em66Y-teeoABHUBzZDpaDUGvRHNgPgvESjzTE7yfkRADRw-Ykdcy2UQiVmbHmRxxaLuyF1aaRcLPL40PmxCcWiGf74bXFPXYrUNv2mqLfFqo9T2Pe3fUh53IF9cXPKjta-zXR2qHP26-LHz-VVeX17uVourssgrRpLQVGTjlpRrK3ikaInFKqO1gsjCXVcr4kLMIqrwCtdBbRWBW8NN6q2UszZ99fcp6nuKAbqx8G37mloOj9sXfKN-3fSNw9uk56drBDRVruAr4eAIf2eKI-ua3KgtvU9pSk7rKAyKIUW_0cNVhYsSrND4RUNQ8p5oPX7RQhur8m9aXIHTbuVL39_8r7w5kW8AEBIkJA</recordid><startdate>20151015</startdate><enddate>20151015</enddate><creator>Miller, Marina</creator><creator>Beppu, Andrew</creator><creator>Rosenthal, Peter</creator><creator>Pham, Alexa</creator><creator>Das, Sudipta</creator><creator>Karta, Maya</creator><creator>Song, Dae Jin</creator><creator>Vuong, Christine</creator><creator>Doherty, Taylor</creator><creator>Croft, Michael</creator><creator>Zuraw, Bruce</creator><creator>Zhang, Xu</creator><creator>Gao, Xiang</creator><creator>Aceves, Seema</creator><creator>Chouiali, Fazila</creator><creator>Hamid, Qutayba</creator><creator>Broide, David H</creator><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>7X8</scope><scope>7T5</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20151015</creationdate><title>Fstl1 Promotes Asthmatic Airway Remodeling by Inducing Oncostatin M</title><author>Miller, Marina ; 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In this article, we show that follistatin-like 1 (Fstl1), a mediator not previously associated with asthma, is highly expressed by macrophages in the lungs of humans with severe asthma. Chronic allergen-challenged Lys-Cre(tg) /Fstl1(Δ/Δ) mice in whom Fstl1 is inactivated in macrophages/myeloid cells had significantly reduced airway remodeling and reduced levels of oncostatin M (OSM), a cytokine previously not known to be regulated by Fstl1. The importance of the Fstl1 induction of OSM to airway remodeling was demonstrated in murine studies in which administration of Fstl1 induced airway remodeling and increased OSM, whereas administration of an anti-OSM Ab blocked the effect of Fstl1 on inducing airway remodeling, eosinophilic airway inflammation, and airway hyperresponsiveness, all cardinal features of asthma. Overall, these studies demonstrate that the Fstl1/OSM pathway may be a novel pathway to inhibit airway remodeling in severe human asthma.</abstract><cop>United States</cop><pmid>26355153</pmid><doi>10.4049/jimmunol.1501105</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Airway Remodeling - drug effects Airway Remodeling - genetics Airway Remodeling - immunology Animals Antibodies - immunology Antibodies - pharmacology Asthma - genetics Asthma - immunology Asthma - pathology Female Follistatin-Related Proteins - genetics Follistatin-Related Proteins - immunology Humans Macrophages - immunology Macrophages - pathology Male Mice Oncostatin M - genetics Oncostatin M - immunology Signal Transduction - drug effects Signal Transduction - genetics Signal Transduction - immunology |
| title | Fstl1 Promotes Asthmatic Airway Remodeling by Inducing Oncostatin M |
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