Present address: Center for International Health Research, Rhode Island Hospital, Providence, RI, USA.
The Pro-Inflammatory Role of Adiponectin at the Maternal–Fetal Interface
Article first published online: 19 JAN 2011
© 2011 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 66, Issue 2, pages 128–136, August 2011
How to Cite
McDonald, E. A. and Wolfe, M. W. (2011), The Pro-Inflammatory Role of Adiponectin at the Maternal–Fetal Interface. American Journal of Reproductive Immunology, 66: 128–136. doi: 10.1111/j.1600-0897.2010.00971.x
- Issue published online: 7 JUL 2011
- Article first published online: 19 JAN 2011
- Submitted November 10, 2010; accepted December 13, 2010.
- immune response;
Citation McDonald EA, Wolfe MW. The pro-inflammatory role of adiponectin at the maternal–fetal interface. Am J Reprod Immunol 2011; 66: 128–136
Problem A successful pregnancy is contingent on maternal tolerance of the immunologically foreign fetus. Prevalent diseases such as preeclampsia arise in part due to an inappropriate immune response by the placenta. A number of molecules have been proposed to temper cellular response to pro-inflammatory mediators, including CD24 and Siglec10.
Methods Cytotrophoblast cells from healthy term placentas were treated with adiponectin in vitro and analyzed with qPCR and ELISA-based assays. Immunohistochemistry was performed on term villous sections and cultured trophoblasts.
Results Treatment with adiponectin increased expression of IL-1β and IL-8. Term villi express CD24 in cytotrophoblasts and the syncytiotrophoblast, and Siglec10 by the syncytiotrophoblast. Treatment of trophoblast cells with adiponectin increased Siglec10 expression.
Conclusion These data describe a role for adiponectin in enhancing pro-inflammatory signals in in vitro syncytialized trophoblasts. Additionally, this represents the first time the CD24/Siglec10 pathway has been implicated in a trophoblast response to a pro-inflammatory mediator.