In their recent study, Djurovic et al.1 reported maternal levels of various cytokines with putative roles in the pathophysiology of impaired placentation and pre-eclampsia. Of these cytokines, they demonstrated that interleukin-10 (IL-10), an anti-inflammatory cytokine, was mainly undetectable in maternal plasma and that at approximately 18 weeks of pregnancy, there were no differences in levels between women with a normal pregnancy and those who subsequently developed pre-eclampsia. This is in contrast to previous reports of depressed placental IL-10 levels in association with established pre-eclampsia2 and reduced decidual IL-10 mRNA expression in association with fetal intrauterine growth retardation3, another pregnancy complication characterised by impaired placentation. Both of these findings would be in keeping with the accepted immunosuppressive roles of IL-10 at the maternal–placental interface. To date, there have been no reports of maternal serum IL-10 levels in intrauterine growth retardation pregnancies.
Thus, to study the ontogeny of maternal IL-10 in normal pregnancy and to explore its possible use as a diagnostic marker of intrauterine growth retardation, we measured IL-10 in serial third trimester maternal serum samples collected at ∼24, 28, 32 and 36 weeks of gestation from six women with normal singleton pregnancies and in serum collected from 13 women with a diagnosis of intrauterine growth retardation, whose gestational ages were within the range of the normal pregnancy group. The measurement of IL-10 was done using a high sensitivity commercial enzyme-linked immunoassay (R&D Systems, Minneapolis, Minnesota, USA) with a detection range of 0.78–50 pg/mL. We found that IL-10 was inconsistently detected in serum from both normal and intrauterine growth retardation groups. No IL-10 was detected in two out of six samples from the normal group or in 6 out of 13 samples from the intrauterine growth retardation group. The levels were lower than those reported previously1,2 with a median (range) of 0.00 (0.00–8.40) and 0.26 (0.00–1.83) pg/mL for normal and intrauterine growth retardation groups, respectively (P= 0.85, Mann Whitney U test).
We believe that these findings, together with those from the previous studies, suggest that while IL-10 may well have important anti-inflammatory (Th2-type) roles at the maternal–fetal interface in pregnancy and that while placental and decidual production of IL-10 may be impaired in association with pre-eclampsia and intrauterine growth retardation, these possibilities are not reflected in circulating maternal serum levels in pregnancies complicated by either pre-eclampsia or intrauterine growth retardation. The inability to detect consistently IL-10 in maternal serum in normal and complicated pregnancies, despite using highly sensitive assays, suggests that the potential use of IL-10 as a clinical diagnostic marker in pregnancy should be approached with caution.