Placental tissue interleukin-10 receptor distribution In pre-eclampsia

PROBLEM: Reduced placental (trophoblast) cytokine interleukin-10 (IL-10) occurs in human pre-eclampsia. Along with an increase in inflammatory cytokines this may play an important role in the development of hypertension in pregnancy. It is not clear whether the changes in placental IL-10 are due to a change in the placental cell production of IL-10 or a result of changes in cytokine receptor status in adjacent tissues. This study is aimed at qualifying the presence and distribution of IL-10 receptors in women with a pre-eclamptic outcome compared to normal pregnancy and gestational hypertension. METHOD OF STUDY: Patients at the KGV Hospital, Sydney was selected for the study. Placentas were collected fresh and paraffin serial sections made. Sections were stained with IL-10 receptor antibody (10 μg/mL) using avidin–biotin immunohistochemistry. Tissues of patients with pre-eclampsia (n = 11) were compared with normal pregnancy (n = 12). Pre-eclampsia was defined as a blood pressure >140/90 mmHg on two occasions and de novo proteinuria > 300 mg per day which resolved post-partum. The fetal weights, gestational ages and maternal ages at delivery were compared (ANOVA) and the differences in staining of decidual and villous tissues were graded according to density. Statistical comparisons were made using the Kruskal–Wallis test. RESULTS: The groups were similar for maternal gestational age but delivered at earlier gestation and with lower fetal weight. There was significantly less villous cytotrophoblast staining for IL-10 receptor in all groups (P = 0.012) compared to decidual trophoblast cells. There was equal intensity and density of extravillous staining observed in normal pregnancy (45 ± 12%) positive cells compared to pre-eclampsia (27 ± 12%). CONCLUSION: IL-10 receptors are present in greater concentration in the extravillous (decidual) trophoblast compared to villi. The decrease in IL-10 produced by trophoblast cells in pre-eclampsia is not explained by a difference in the IL-10 receptor distribution compared to normal pregnancy.