Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/23198
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Type: Journal article
Title: Essential role for IL-10 in resistance to lipopolysaccharide-induced preterm labor in mice
Author: Robertson, S.
Skinner, R.
Care, A.
Citation: Journal of Immunology, 2006; 177(7):4888-4896
Publisher: Amer Assoc Immunologists
Issue Date: 2006
ISSN: 0022-1767
1550-6606
Statement of
Responsibility: 
Sarah A. Robertson, Rebecca J. Skinner, and Alison S. Care
Abstract: 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- and IL-6 was evident in the serum, uterus, and placenta of IL-10–/– mice, and TNF- and IL-6 mRNA expression was elevated in the uterus and placenta, but not the fetus. Serum IL-1, IFN-, 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.
Keywords: Uterus; Placenta; Animals; Mice; Mice, Mutant Strains; Inflammation; Lipopolysaccharides; Tumor Necrosis Factor-alpha; Receptors, Tumor Necrosis Factor, Type II; Protein Subunits; RNA, Messenger; Interleukin-1; Interleukin-6; Interleukin-10; Interleukin-12; Immunoassay; Reverse Transcriptase Polymerase Chain Reaction; Pregnancy; Mutation; Female; Obstetric Labor, Premature; Interleukin-12 Subunit p40; Interferon-gamma
Description: Copyright © 2006 by The American Association of Immunologists, Inc.
RMID: 0020061429
DOI: 10.4049/jimmunol.177.7.4888
Published version: http://www.jimmunol.org/cgi/content/abstract/177/7/4888
Appears in Collections:Obstetrics and Gynaecology publications

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