Placental deficiency of interleukin-10 (IL-10) in preeclampsia 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 maternal-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 (-1082) A promoter polymorphism contributes to lower concentrations. In a prospective case-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 preeclampsia 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.
Makris
A
A
Vascular Immunology Laboratory, Heart Research Institute, 145 Missenden Road, Camperdown 2050, New South Wales, Australia. a.makris@hri.org.au
Xu
B
B
Yu
B
B
Thornton
C
C
Hennessy
A
A
D000328:Adult; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000097:blood / Q000172:deficiency* / Q000235:genetics; D010920:Placenta / Q000378:metabolism*; D011110:Polymorphism, Genetic; D011225:Pre-Eclampsia / Q000235:genetics / Q000378:metabolism*; D011247:Pregnancy; D011401:Promoter Regions, Genetic
D016753:Interleukin-10