{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:48:48Z","timestamp":1792788528652,"version":"4.5.0"},"reference-count":81,"publisher":"The Company of Biologists","issue":"10","license":[{"start":{"date-parts":[[2021,2,8]],"date-time":"2021-02-08T00:00:00Z","timestamp":1612742400000},"content-version":"vor","delay-in-days":496,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["DK097335"],"award-info":[{"award-number":["DK097335"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HD081121"],"award-info":[{"award-number":["HD081121"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Stead Family Department of Pediatrics"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,10,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Fetal exposure to chorioamnionitis can impact the outcomes of the developing fetus both at the time of birth and in the subsequent neonatal period. Infants exposed to chorioamnionitis have a higher incidence of gastrointestinal (GI) pathology, including necrotizing enterocolitis (NEC); however, the mechanism remains undefined. To simulate the fetal exposure to maternal inflammation (FEMI) induced by chorioamnionitis, pregnant mice (C57BL\/6J, IL-6\u2212\/\u2212, RAG\u2212\/\u2212 or TNFR1\u2212\/\u2212) were injected intraperitoneally on embryonic day (E)15.5 with lipopolysaccharide (LPS; 100\u2005\u00b5g\/kg body weight). Pups were delivered at term, and reared to postnatal day (P)0, P7, P14, P28 or P56. Serum and intestinal tissue samples were collected to quantify growth, inflammatory markers, histological intestinal injury, and goblet and Paneth cells. To determine whether FEMI increased subsequent susceptibility to intestinal injury, a secondary dose of LPS (100\u2005\u00b5g\/kg body weight) was given on P5, prior to tissue harvesting on P7. FEMI had no effect on growth of the offspring or their small intestine. FEMI significantly decreased both goblet and Paneth cell numbers while simultaneously increasing serum levels of IL-1\u03b2, IL-10, KC\/GRO (CXCL1 and CXCL2), TNF and IL-6. These alterations were IL-6 dependent and, importantly, increased susceptibility to LPS-induced intestinal injury later in life. Our data show that FEMI impairs normal intestinal development by decreasing components of innate immunity and simultaneously increasing markers of inflammation. These changes increase susceptibility to intestinal injury later in life and provide novel mechanistic data to potentially explain why preterm infants exposed to chorioamnionitis prior to birth have a higher incidence of NEC and other GI disorders.<\/jats:p>","DOI":"10.1242\/dmm.040808","type":"journal-article","created":{"date-parts":[[2019,9,19]],"date-time":"2019-09-19T09:05:14Z","timestamp":1568883914000},"source":"Crossref","is-referenced-by-count":36,"title":["Fetal exposure to maternal inflammation interrupts murine intestinal development and increases susceptibility to neonatal intestinal injury"],"prefix":"10.1242","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5936-0463","authenticated-orcid":false,"given":"Timothy G.","family":"Elgin","sequence":"first","affiliation":[{"name":"University of Iowa 1 Department of Pediatrics , , Iowa City, IA 52242 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin M.","family":"Fricke","sequence":"additional","affiliation":[{"name":"University of Iowa 2 Department of Obstetrics and Gynecology , , Iowa City, IA 52242 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huiyu","family":"Gong","sequence":"additional","affiliation":[{"name":"University of Iowa 1 Department of Pediatrics , , Iowa City, IA 52242 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8751-6146","authenticated-orcid":false,"given":"Jeffrey","family":"Reese","sequence":"additional","affiliation":[{"name":"Vanderbilt University 3 Department of Pediatrics , , Nashville, TN 37232 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Mills","sequence":"additional","affiliation":[{"name":"University of California Davis 4 Department of Food Science and Technology , , Davis, CA 95616 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen M.","family":"Kalantera","sequence":"additional","affiliation":[{"name":"University of California Davis 4 Department of Food Science and Technology , , Davis, CA 95616 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7453-5022","authenticated-orcid":false,"given":"Mark A.","family":"Underwood","sequence":"additional","affiliation":[{"name":"University of California Davis 5 Department of Pediatrics , , Sacramento, CA 95817 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4321-723X","authenticated-orcid":false,"given":"Steven J.","family":"McElroy","sequence":"additional","affiliation":[{"name":"University of Iowa 1 Department of Pediatrics , , Iowa City, IA 52242 , USA"},{"name":"University of Iowa 6 Department of Microbiology and Immunology , , Iowa City, IA 52242 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2019,10,21]]},"reference":[{"key":"2024061302142206100_DMM040808C1","doi-asserted-by":"publisher","first-page":"12","DOI":"10.1016\/j.siny.2011.09.001","article-title":"Intrauterine infection and preterm labor","volume":"17","author":"Agrawal","year":"2012","journal-title":"Semin. 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