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These effects of IL-1 were diminished, and SP-C mRNA was suppressed additively in the presence of tumor necrosis factor (TNF)-\u03b1 and either LPS or interferon (IFN)-\u03b3. LPS, TNF-\u03b1, or IFN-\u03b3 had no effect alone. In explants from the term fetus and the newborn, LPS, IL-1\u03b1, and TNF-\u03b1 additively suppressed the SPs. LPS acutely induced IL-1\u03b1 in alveolar macrophages in mature lung but not in the immature lung. IFN-\u03b3 that generally has low expression in intrauterine infection decreased the age dependence of the other agonists' effects on SPs. The present study serves to explain the variation of the pulmonary outcome after an inflammatory insult. We propose that IL-1 from extrapulmonary sources induces the SPs in premature lung and is responsible for the decreased risk of RDS in intra-amniotic infection.<\/jats:p>","DOI":"10.1152\/ajplung.00274.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:16:38Z","timestamp":1425413798000},"page":"L803-L810","source":"Crossref","is-referenced-by-count":42,"title":["Regulation of surfactant proteins by LPS and proinflammatory cytokines in fetal and newborn lung"],"prefix":"10.1152","volume":"282","author":[{"given":"Outi","family":"V\u00e4yrynen","sequence":"first","affiliation":[{"name":"Department of Pediatrics and Biocenter Oulu, University of Oulu, Oulu FIN-90014, Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Virpi","family":"Glumoff","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Biocenter Oulu, University of Oulu, Oulu FIN-90014, 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