{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T13:13:40Z","timestamp":1789996420426,"version":"4.0.1"},"reference-count":73,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2013,8,1]],"date-time":"2013-08-01T00:00:00Z","timestamp":1375315200000},"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":[[2013,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Very low birth weight preterm newborns are susceptible to the development of debilitating inflammatory diseases, many of which are associated with chorioamnionitis. To define the effects of chorioamnionitis on the fetal immune system, IL-1\u03b2 was administered intra-amniotically at \u223c80% gestation in rhesus monkeys. IL-1\u03b2 caused histological chorioamnionitis, as well as lung inflammation (infiltration of neutrophils or monocytes in the fetal airways). There were large increases in multiple proinflammatory cytokine mRNAs in the lungs at 24 h postadministration, which remained elevated relative to controls at 72 h. Intra-amniotic IL-1\u03b2 also induced the sustained expression of the surfactant proteins in the lungs. Importantly, IL-1\u03b2 significantly altered the balance between inflammatory and regulatory T cells. Twenty-four hours after IL-1\u03b2 injection, the frequency of CD3+CD4+FOXP3+ T cells was decreased in lymphoid organs. In contrast, IL-17A\u2013producing cells (CD3+CD4+, CD3+CD4\u2212, and CD3\u2212CD4\u2212 subsets) were increased in lymphoid organs. The frequency of IFN-\u03b3\u2013expressing cells did not change. In this model of a single exposure to an inflammatory trigger, CD3+CD4+FOXP3+ cells rebounded quickly, and their frequency was increased at 72 h compared with controls. IL-17 expression was also transient. Interestingly, the T cell profile alteration was confined to the lymphoid organs and not to circulating fetal T cells. Together, these results suggest that the chorioamnionitis-induced IL-1\/IL-17 axis is involved in the severe inflammation that can develop in preterm newborns. Boosting regulatory T cells and\/or controlling IL-17 may provide a means to ameliorate these abnormalities.<\/jats:p>","DOI":"10.4049\/jimmunol.1300270","type":"journal-article","created":{"date-parts":[[2013,6,22]],"date-time":"2013-06-22T01:53:34Z","timestamp":1371866014000},"page":"1102-1109","source":"Crossref","is-referenced-by-count":70,"title":["Intra-Amniotic IL-1\u03b2 Induces Fetal Inflammation in Rhesus Monkeys and Alters the Regulatory T Cell\/IL-17 Balance"],"prefix":"10.1093","volume":"191","author":[{"given":"Suhas G","family":"Kallapur","sequence":"first","affiliation":[{"name":"Perinatal Institute, Cincinnati Children\u2019s Hospital Medical Center, University of Cincinnati , Cincinnati, OH 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pietro","family":"Presicce","sequence":"additional","affiliation":[{"name":"Perinatal Institute, Cincinnati Children\u2019s Hospital Medical Center, University of Cincinnati , Cincinnati, OH 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paranthaman","family":"Senthamaraikannan","sequence":"additional","affiliation":[{"name":"Perinatal Institute, Cincinnati Children\u2019s Hospital Medical Center, University of Cincinnati , Cincinnati, OH 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel","family":"Alvarez","sequence":"additional","affiliation":[{"name":"Perinatal Institute, Cincinnati Children\u2019s Hospital Medical Center, University of Cincinnati , Cincinnati, OH 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alice F","family":"Tarantal","sequence":"additional","affiliation":[{"name":"California National Primate Research Center, University of California , Davis, Davis, CA 95616"},{"name":"Department of Pediatrics, School of Medicine, University of California , Davis, Davis, CA 95818"},{"name":"Department of Cell Biology and Human Anatomy, School of Medicine, University of California , Davis, Davis, CA 95616"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa M","family":"Miller","sequence":"additional","affiliation":[{"name":"California National Primate Research Center, University of California , Davis, Davis, CA 95616"},{"name":"Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California , Davis, Davis, CA 95616"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan H","family":"Jobe","sequence":"additional","affiliation":[{"name":"Perinatal Institute, Cincinnati Children\u2019s Hospital Medical Center, University of Cincinnati , Cincinnati, OH 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claire A","family":"Chougnet","sequence":"additional","affiliation":[{"name":"Perinatal Institute, Cincinnati Children\u2019s Hospital Medical Center, University of Cincinnati , Cincinnati, OH 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,8,1]]},"reference":[{"key":"2025032405120788300_r1","doi-asserted-by":"crossref","first-page":"443","DOI":"10.1542\/peds.2009-2959","article-title":"Neonatal outcomes of extremely preterm infants from the NICHD Neonatal Research Network","volume":"126","author":"Stoll","year":"2010","journal-title":"Pediatrics"},{"key":"2025032405120788300_r2","doi-asserted-by":"crossref","first-page":"394","DOI":"10.1203\/PDR.0b013e3181d01a36","article-title":"Perinatal systemic inflammatory response syndrome and retinopathy of prematurity","volume":"67","author":"Sood","year":"2010","journal-title":"Pediatr. 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