| pubmed-article:16982931 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16982931 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:16982931 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:16982931 | lifeskim:mentions | umls-concept:C0022876 | lld:lifeskim |
| pubmed-article:16982931 | lifeskim:mentions | umls-concept:C0085295 | lld:lifeskim |
| pubmed-article:16982931 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:16982931 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:16982931 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:16982931 | pubmed:dateCreated | 2006-9-19 | lld:pubmed |
| pubmed-article:16982931 | pubmed:abstractText | 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(-/-)) 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(-/-) mice than in IL-10(+/+) mice. Surviving fetuses in IL-10(-/-) mice exhibited fetal growth restriction at lower doses of LPS than IL-10(+/+) mice. Marked elevation of LPS-induced immunoactive TNF-alpha and IL-6 was evident in the serum, uterus, and placenta of IL-10(-/-) mice, and TNF-alpha and IL-6 mRNA expression was elevated in the uterus and placenta, but not the fetus. Serum IL-1alpha, IFN-gamma, 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(-/-) 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. | lld:pubmed |
| pubmed-article:16982931 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16982931 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16982931 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16982931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16982931 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16982931 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16982931 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:16982931 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:16982931 | pubmed:author | pubmed-author:RobertsonSara... | lld:pubmed |
| pubmed-article:16982931 | pubmed:author | pubmed-author:SkinnerRebecc... | lld:pubmed |
| pubmed-article:16982931 | pubmed:author | pubmed-author:CareAlison... | lld:pubmed |
| pubmed-article:16982931 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16982931 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16982931 | pubmed:volume | 177 | lld:pubmed |
| pubmed-article:16982931 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16982931 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16982931 | pubmed:pagination | 4888-96 | lld:pubmed |
| pubmed-article:16982931 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:16982931 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16982931 | pubmed:articleTitle | Essential role for IL-10 in resistance to lipopolysaccharide-induced preterm labor in mice. | lld:pubmed |
| pubmed-article:16982931 | pubmed:affiliation | Research Centre for Reproductive Health and Department of Obstetrics and Gynecology, University of Adelaide, Adelaide, SA 5005, Australia. sarah.robertson@adelaide.edu.au | lld:pubmed |
| pubmed-article:16982931 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16982931 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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