Placental deficiency of Interleukin-10 (IL-10) inpreeclampsia and its relationship to an IL10 Promoter polymorphism

The placenta is pivotal in the acceptance of the feto-placental unit by the maternal immune system. Imbalance at the maternalââ"šÂ¬Ã¢â‚¬Å“fetal interface of tissue pro- and anti-inflammatory cytokines may be partly involved in disease causation. Previous work has shown conflicting levels of IL-10. IL-10 levels have been shown to increase, decrease, or remain unchanged in women with preeclampsia. This study examines the difference in serum and placental IL-10 expression in women with preeclampsia and investigates if the IL10 (âË" Ã¢â‚¬â„¢1082) A promoter polymorphism contributes to lower concentrations. In a prospective caseââ"šÂ¬Ã¢â‚¬Å“control study of 12 women with preeclampsia and 31 controls we assessed serum IL-10 by ELISA, placental mRNA by quantitative PCR and protein by immunohistochemistry as well as placental IL10 promoter genotype. Comparisons were made with non-parametric tests where necessary and chi-square. We found a significant reduction in placental IL-10 mRNA and protein expression in women with eeclampsia compared to controls. Women with the AA IL-10 promoter genotype expressed less placental IL-10 mRNA compared to women with AG or GG genotype. There was no difference in serum IL-10 concentrations between different genotypes. Preeclampsia is associated with a deficiency of placental IL-10. Placental AA genotype in the promoter region results in significantly less placental IL-10.