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Notably, females with cystic fibrosis (CF) suffer worse outcomes, particularly in the setting of\n                    <jats:named-content content-type=\"genus-species\">Pseudomonas aeruginosa<\/jats:named-content>\n                    infection. Sex hormones have been implicated in experimental and clinical studies; however, immune mechanisms responsible for this sex-based disparity are unknown and the specific sex hormone target for therapeutic manipulation has not been identified. The objective of this study was to assess mechanisms behind the impact of female sex hormones on host immune responses to\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    . We used wild-type and CF mice, which we hormone manipulated, inoculated with\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    , and then examined for outcomes and inflammatory responses. Neutrophils isolated from mice and human subjects were tested for responses to\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    . We found that female mice inoculated with\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    died earlier and showed slower bacterial clearance than males (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.0001). Ovariectomized females supplemented with 17\u03b2-estradiol succumbed to\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    challenge earlier than progesterone- or vehicle-supplemented mice (\n                    <jats:italic>P<\/jats:italic>\n                    = 0.0003). 17\u03b2-Estradiol-treated ovariectomized female mice demonstrated increased lung levels of inflammatory cytokines, and when rendered neutropenic the mortality difference was abrogated. Neutrophils treated with 17\u03b2-estradiol demonstrated an enhanced oxidative burst but decreased\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    killing and earlier cell necrosis. The estrogen receptor (ER) antagonist ICI 182,780 improved survival in female mice infected with\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    and restored neutrophil function. We concluded that ER antagonism rescues estrogen-mediated neutrophil dysfunction and improves survival in response to\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    . ER-mediated processes may explain the sex-based mortality gap in CF and other inflammatory lung illnesses, and the ER blockade represents a rational therapeutic strategy.\n                  <\/jats:p>","DOI":"10.1128\/iai.00422-17","type":"journal-article","created":{"date-parts":[[2017,8,7]],"date-time":"2017-08-07T20:55:25Z","timestamp":1502139325000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":64,"title":["17\u03b2-Estradiol Dysregulates Innate Immune Responses to Pseudomonas aeruginosa Respiratory Infection and Is Modulated by Estrogen Receptor Antagonism"],"prefix":"10.1128","volume":"85","author":[{"given":"Shadaan","family":"Abid","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ShangKui","family":"Xie","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moumita","family":"Bose","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip W.","family":"Shaul","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lance S.","family":"Terada","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven L.","family":"Brody","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip J.","family":"Thomas","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John A.","family":"Katzenellenbogen","sequence":"additional","affiliation":[{"name":"Department of Chemistry, University of Illinois at Urbana\u2014Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sung Hoon","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Chemistry, University of Illinois at Urbana\u2014Champaign, Urbana, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David E.","family":"Greenberg","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raksha","family":"Jain","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1210\/er.2010-0031"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/resp.12702"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2010.06.018"},{"key":"e_1_3_3_5_2","first-page":"1","article-title":"Trends in asthma prevalence, health care use, and mortality in the United States, 2001\u20132010","volume":"94","author":"Akinbami LJ","year":"2012","unstructured":"Akinbami LJ Moorman JE Bailey C Zahran HS King M Johnson CA Liu X . 2012. 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