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The Pro‐Inflammatory Role of Adiponectin at the Maternal–Fetal Interface
Author(s) -
McDonald Emily A.,
Wolfe Michael W.
Publication year - 2011
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2010.00971.x
Subject(s) - cytotrophoblast , syncytiotrophoblast , trophoblast , adiponectin , placenta , preeclampsia , immune system , immunology , biology , fetus , adipokine , endocrinology , medicine , andrology , pregnancy , leptin , insulin resistance , genetics , insulin , obesity
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.