{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T05:16:28Z","timestamp":1787807788908,"version":"build-2784847793"},"reference-count":62,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2006,10,1]],"date-time":"2006-10-01T00:00:00Z","timestamp":1159660800000},"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":[[2006,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>IL-10 is highly expressed in the uterus and placenta and is implicated in controlling inflammation-induced pathologies of pregnancy. To investigate the role of IL-10 in regulating preterm labor, the response of IL-10 null mutant mice to low-dose LPS in late gestation was evaluated. When IL-10 null mutant C57BL\/6 (IL-10\u2212\/\u2212) and control (IL-10+\/+) mice were administered LPS on day 17 of pregnancy, the dose of LPS required to elicit 50% preterm fetal loss was 10-fold lower in IL-10\u2212\/\u2212 mice than in IL-10+\/+ mice. Surviving fetuses in IL-10\u2212\/\u2212 mice exhibited fetal growth restriction at lower doses of LPS than IL-10+\/+ mice. Marked elevation of LPS-induced immunoactive TNF-\u03b1 and IL-6 was evident in the serum, uterus, and placenta of IL-10\u2212\/\u2212 mice, and TNF-\u03b1 and IL-6 mRNA expression was elevated in the uterus and placenta, but not the fetus. Serum IL-1\u03b1, IFN-\u03b3, and IL-12p40 were increased and soluble TNFRII was diminished in the absence of IL-10, with these changes also reflected in the gestational tissues. Administration of rIL-10 to IL-10\u2212\/\u2212 mice attenuated proinflammatory cytokine synthesis and alleviated their increased susceptibility to preterm loss. Exogenous IL-10 also protected IL-10+\/+ mice from fetal loss. These data show that IL-10 modulates resistance to inflammatory stimuli by down-regulating proinflammatory cytokines in the uterus and placenta. Abundance of endogenous IL-10 in gestational tissues is therefore identified as a critical determinant of resistance to preterm labor, and IL-10 may provide a useful therapeutic agent in this common condition.<\/jats:p>","DOI":"10.4049\/jimmunol.177.7.4888","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T13:15:01Z","timestamp":1397826901000},"page":"4888-4896","source":"Crossref","is-referenced-by-count":175,"title":["Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice"],"prefix":"10.1093","volume":"177","author":[{"given":"Sarah A","family":"Robertson","sequence":"first","affiliation":[{"name":"Research Centre for Reproductive Health and Department of Obstetrics and Gynecology, University of Adelaide , Adelaide ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca J","family":"Skinner","sequence":"additional","affiliation":[{"name":"Research Centre for Reproductive Health and Department of Obstetrics and Gynecology, University of Adelaide , Adelaide ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alison S","family":"Care","sequence":"additional","affiliation":[{"name":"Research Centre for Reproductive Health and Department of Obstetrics and Gynecology, University of Adelaide , Adelaide ,","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,10,1]]},"reference":[{"key":"2026020209095405200_R1","first-page":"817","volume-title":"Am. 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