Interestingly, in

IgA nephropathy, glomerular deposition of ficolin-2 with local lectin pathway activation was associated with more severe renal disease [37]. According to our findings, pregnant women with low circulating levels of ficolin-2 or ficolin-3 have an increased risk for pre-eclampsia. Low ficolin-2 and ficolin-3 levels have already been linked to various pathological conditions, such as combined allergic and infectious respiratory disease in children [38,39], bronchiectasis [40], prematurity, low birth weight and perinatal infections [41], sarcoidosis [42], susceptibility to fever and neutropenia in pediatric cancer patients [43] and to neonatal sepsis [44]. Moreover, our research group has demonstrated recently that low ficolin-3 levels in early follow-up serum samples Crizotinib ic50 are related to the severity and unfavourable outcome of acute ischaemic stroke [45]. Genetic variations were shown to affect ligand binding or circulating levels of ficolins [46–48] and to associate with several disorders, including rheumatic fever and chronic rheumatic heart disease [49], bacterial and cytomegalovirus infections after orthotopic liver transplantation [50,51], and even immunodeficiency [52]. As pre-eclampsia is a multi-factorial disease with genetic components, the role of ficolin gene polymorphisms should be examined in buy BMN 673 the

future in the risk of this pregnancy-specific disorder. In our study, the similar plasma ficolin-2 and ficolin-3 levels of pre-eclamptic patients regardless of the severity, the time of onset of the disease or the presence click here of fetal growth restriction might be explained by the complex aetiology of pre-eclampsia. Several genetic, behavioural and environmental factors need to interact to produce the complete picture of this pregnancy-specific disorder. We reported various genetic and soluble factors that were associated with the severity

or complications of pre-eclampsia, including HELLP syndrome and fetal growth restriction [53–56]. Nevertheless, it is also possible that the relatively small sample size of this study prevented the detection of an effect in the subgroup analyses. Although pre-eclampsia is predominantly a disease of primiparas, multiparous women, especially with advanced age or over weight, can also be affected, as in our cases. In conclusion, circulating levels of ficolin-2 are decreased in the third trimester of normal pregnancy. There is a further decrease in plasma ficolin-2 concentrations in pre-eclampsia, which might contribute to the development of the maternal syndrome of the disease through impaired removal of the trophoblast-derived material released into the maternal circulation by the hypoxic and oxidatively stressed pre-eclamptic placenta. We thank Veronika Makó, László Cervenak and Levente Lázár for measuring plasma von Willebrand factor antigen and cell-free fetal DNA concentrations.