{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T04:45:19Z","timestamp":1784090719553,"version":"3.55.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2010,2,1]],"date-time":"2010-02-01T00:00:00Z","timestamp":1264982400000},"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":[[2010,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Little is known about the influence of maternal inflammation on neonatal outcome. Production of IL-1\u03b2 in the lungs of newborn infants is associated with bronchopulmonary dysplasia. Using bitransgenic (bi-TG) mice in which human (h) IL-1\u03b2 is expressed with a doxycycline-inducible system controlled by the Clara cell secretory protein promoter, we have shown that hIL-1\u03b2 expression causes a bronchopulmonary dysplasia\u2013like illness in infant mice. To study the hypothesis that maternal hIL-1\u03b2 production modifies the response of the newborn to hIL-1\u03b2, doxycycline was administered to bi-TG and control dams from Embryonic Day 0, inducing production of hIL-1\u03b2 by the bi-TG dams before hIL-1\u03b2 production started in their bi-TG fetuses, or from Embryonic Day 15, inducing simultaneous production of hIL-1\u03b2 by both the bi-TG dams and their bi-TG fetuses. In addition to the lungs, hIL-1\u03b2 was expressed at low levels in the uteri of bi-TG dams. Maternal inflammation preceding fetal inflammation increased the survival and growth of hIL-1\u03b2\u2013expressing pups, enhanced alveolarization, and protected the airways against remodeling and goblet cell hyperplasia. Maternal hIL-1\u03b2 production preceding fetal hIL-1\u03b2 production caused silencing of several inflammatory genes, including CXC and CC chemokines, murine IL-1\u03b2, serum amyloid A3, and Toll-like receptors 2 and 4, and suppressed the expression of chitinase-like lectins Ym1 and Ym2 in the lungs of infant mice. Maternal inflammation protects the newborn against subsequent hIL-1\u03b2\u2013induced lung inflammation and injury. In contrast, induction of hIL-1\u03b2 production simultaneously in bi-TG dams and their fetuses offered no protection against inflammatory lung disease in the neonate.<\/jats:p>","DOI":"10.1165\/rcmb.2008-0287oc","type":"journal-article","created":{"date-parts":[[2009,5,1]],"date-time":"2009-05-01T20:44:46Z","timestamp":1241210686000},"page":"149-160","source":"Crossref","is-referenced-by-count":12,"title":["Maternal IL-1\u03b2 Production Prevents Lung Injury in a Mouse Model of Bronchopulmonary Dysplasia"],"prefix":"10.1093","volume":"42","author":[{"given":"Erica","family":"B\u00e4ckstr\u00f6m","sequence":"first","affiliation":[{"name":"Department of Pediatrics, University of Gothenburg, Gothenburg, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Urpo","family":"Lappalainen","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Gothenburg, Gothenburg, 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