{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T12:00:53Z","timestamp":1790164853908,"version":"4.1.0"},"reference-count":28,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,3,5]],"date-time":"2014-03-05T00:00:00Z","timestamp":1393977600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Rep Immunol"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:sec><jats:title>Problem<\/jats:title><jats:p>Exposure to intrauterine inflammation, associated with preterm birth, has been linked to a devastating spectrum of neurobehavioral disorders. Mechanisms of this injury are unknown. Using a mouse model of intrauterine inflammation, we have observed a disruption of fetal neuronal morphology along with a marked elevation of interleukin (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>)\u20101\u03b2 in the fetal brain and placenta. In this study, we hypothesized that <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 plays a key role in perinatal brain injury.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method of study<\/jats:title><jats:p>Utilizing a mouse model of inflammation\u2010induced preterm birth, we investigated the role of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 in fetal cortical injury as well as preterm birth. In these studies, dams received systemic treatment with <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 receptor antagonist prior to administration of intrauterine inflammation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Systemic maternal antagonism of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 improved fetal cortical neuronal injury associated with the exposure to intrauterine inflammation, without affecting the phenotype of preterm birth. <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 receptor antagonist blocked activation of neuronal nitric oxide synthase in perinatal cortex, a key enzyme implicated in neurotoxicity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our data suggest that fetal cortical brain injury and preterm birth may occur by divergent mechanisms. Furthermore, our studies indicate maternal administration of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 receptor antagonist (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>) blocked neuronal nitric oxide synthase activation observed in the brain cortex and, we speculate, that this alteration in activation leads to demonstrated decreased neurotoxicity.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aji.12216","type":"journal-article","created":{"date-parts":[[2014,3,5]],"date-time":"2014-03-05T07:02:37Z","timestamp":1394002957000},"page":"418-426","source":"Crossref","is-referenced-by-count":92,"title":["<scp>IL<\/scp>\u20101 Receptor Blockade Prevents Fetal Cortical Brain Injury but Not Preterm Birth in a Mouse Model of Inflammation\u2010Induced Preterm Birth and Perinatal Brain Injury"],"prefix":"10.1111","volume":"71","author":[{"given":"Kirstin","family":"Leitner","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology Maternal and Child Health Research Program University of Pennsylvania Perelman School of Medicine Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mofeedah","family":"Al Shammary","sequence":"additional","affiliation":[{"name":"Department of Gynecology and Obstetrics Integrated Research Center for Fetal Medicine Johns Hopkins University School of Medicine Baltimore MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"McLane","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology Maternal and Child Health Research Program University of Pennsylvania Perelman School of Medicine Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael V.","family":"Johnston","sequence":"additional","affiliation":[{"name":"Department of Neuroscience Kennedy Krieger Institute Baltimore MD USA"},{"name":"Department of Neurology Johns Hopkins University School of Medicine Baltimore MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michal A.","family":"Elovitz","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology Maternal and Child Health Research Program University of Pennsylvania Perelman School of Medicine Philadelphia PA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irina","family":"Burd","sequence":"additional","affiliation":[{"name":"Department of Gynecology and Obstetrics Integrated Research Center for Fetal Medicine Johns Hopkins University School of Medicine Baltimore MD USA"},{"name":"Department of Neuroscience Kennedy Krieger Institute Baltimore MD USA"},{"name":"Department of Neurology Johns Hopkins University School of Medicine Baltimore MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,3,5]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.clp.2008.03.003"},{"key":"e_1_2_6_3_1","unstructured":"HamiltonBE MartinJA VenturaSJ:Births: Preliminary data for 2012. 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