{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T15:03:41Z","timestamp":1792595021054,"version":"4.5.0"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2018,11,1]],"date-time":"2018-11-01T00:00:00Z","timestamp":1541030400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Allergic asthma is a disease initiated by a breach of the lung mucosal barrier and an inappropriate Th2 inflammatory immune response that results in M2 polarization of alveolar macrophages (AM). The number of M2 macrophages in the airway correlates with asthma severity in humans. Sex differences in asthma suggest that sex hormones modify lung inflammation and macrophage polarization. Asthmatic women have more M2 macrophages than asthmatic men and androgens have been used as an experimental asthma treatment. In this study, we demonstrate that although androgen (dihydrotestosterone) reconstitution of castrated mice reduced lung inflammation in a mouse model of allergic lung inflammation, it enhanced M2 polarization of AM. This indicates a cell-specific role for androgens. Dihydrotestosterone also enhanced IL-4\u2013stimulated M2 macrophage polarization in vitro. Using mice lacking androgen receptor (AR) in monocytes\/macrophages (ARfloxLysMCre), we found that male but not female mice exhibited less eosinophil recruitment and lung inflammation due to impaired M2 polarization. There was a reduction in eosinophil-recruiting chemokines and IL-5 in AR-deficient AM. These data reveal an unexpected and novel role for androgen\/AR in promoting M2 macrophage polarization. Our findings are also important for understanding pathology in diseases promoted by M2 macrophages and androgens, such as asthma, eosinophilic esophagitis, and prostate cancer, and for designing new approaches to treatment.<\/jats:p>","DOI":"10.4049\/jimmunol.1800352","type":"journal-article","created":{"date-parts":[[2018,10,10]],"date-time":"2018-10-10T12:06:36Z","timestamp":1539173196000},"page":"2923-2933","source":"Crossref","is-referenced-by-count":141,"title":["Androgen and Androgen Receptor as Enhancers of M2 Macrophage Polarization in Allergic Lung Inflammation"],"prefix":"10.1093","volume":"201","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8714-9091","authenticated-orcid":false,"given":"Mireya","family":"Becerra-D\u00edaz","sequence":"first","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University , Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5526-0916","authenticated-orcid":false,"given":"Ashley B","family":"Strickland","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University , Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1379-2716","authenticated-orcid":false,"given":"Aleksander","family":"Keselman","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University , Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7247-2021","authenticated-orcid":false,"given":"Nicola M","family":"Heller","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University , Baltimore, MD 21205"},{"name":"Allergy and Clinical Immunology, Johns Hopkins University , Baltimore, MD 21205"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2018,11,15]]},"reference":[{"key":"2025030417574885300_r1","doi-asserted-by":"crossref","first-page":"632049","DOI":"10.1155\/2013\/632049","article-title":"Characterization of macrophage phenotypes in three murine models of house-dust-mite-induced asthma","volume":"2013","author":"Draijer","year":"2013","journal-title":"Mediators Inflamm."},{"key":"2025030417574885300_r2","doi-asserted-by":"crossref","first-page":"605","DOI":"10.1038\/mi.2012.74","article-title":"The alveolar macrophages in asthma: a double-edged sword","volume":"5","author":"Balhara","year":"2012","journal-title":"Mucosal Immunol."},{"key":"2025030417574885300_r3","doi-asserted-by":"crossref","first-page":"6","DOI":"10.1186\/1471-2172-13-6","article-title":"Adoptive transfer of IL-4R\u03b1+ macrophages is sufficient to enhance eosinophilic inflammation in a mouse model of allergic lung inflammation","volume":"13","author":"Ford","year":"2012","journal-title":"BMC Immunol."},{"key":"2025030417574885300_r4","doi-asserted-by":"crossref","first-page":"148","DOI":"10.1016\/j.molmed.2005.02.002","article-title":"The role of eosinophils in the pathogenesis of asthma","volume":"11","author":"Kay","year":"2005","journal-title":"Trends Mol. 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