Linked Life Data

16982931

Source:http://linkedlifedata.com/resource/pubmed/id/16982931

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2006-9-19
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4888-96
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16982931-Animals, pubmed-meshheading:16982931-Female, pubmed-meshheading:16982931-Immunoassay, pubmed-meshheading:16982931-Inflammation, pubmed-meshheading:16982931-Interferon-gamma, pubmed-meshheading:16982931-Interleukin-1, pubmed-meshheading:16982931-Interleukin-10, pubmed-meshheading:16982931-Interleukin-12, pubmed-meshheading:16982931-Interleukin-12 Subunit p40, pubmed-meshheading:16982931-Interleukin-6, pubmed-meshheading:16982931-Lipopolysaccharides, pubmed-meshheading:16982931-Mice, pubmed-meshheading:16982931-Mice, Mutant Strains, pubmed-meshheading:16982931-Mutation, pubmed-meshheading:16982931-Obstetric Labor, Premature, pubmed-meshheading:16982931-Placenta, pubmed-meshheading:16982931-Pregnancy, pubmed-meshheading:16982931-Protein Subunits, pubmed-meshheading:16982931-RNA, Messenger, pubmed-meshheading:16982931-Receptors, Tumor Necrosis Factor, Type II, pubmed-meshheading:16982931-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16982931-Tumor Necrosis Factor-alpha, pubmed-meshheading:16982931-Uterus
pubmed:year
2006
pubmed:articleTitle
Essential role for IL-10 in resistance to lipopolysaccharide-induced preterm labor in mice.
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
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't