Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Robertson, S.A. et al.

Robertson, Skinner, Care,

Essential role for IL-10 in resistance to lipopolysaccharide-induced preterm labor in mice.

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.[1]

References

Essential role for IL-10 in resistance to lipopolysaccharide-induced preterm labor in mice. Robertson, S.A., Skinner, R.J., Care, A.S. J. Immunol. (2006) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.