Circulating ficolin-2 and ficolin-3 in normal pregnancy and pre-eclampsia.
Ficolins are soluble molecules of the innate immune system that recognize carbohydrate molecules on microbial pathogens, apoptotic and necrotic cells. They act through two distinct routes: initiating the lectin pathway of complement activation and mediating a primitive opsonophagocytosis. In this study, we measured plasma levels of ficolin-2 and ficolin-3 in 60 pre-eclamptic patients, 60 healthy pregnant women and 59 healthy non-pregnant women by enzyme-linked immunosorbent assay (ELISA). Circulating levels of complement activation products (C4d, C3a, SC5b9), angiogenic factors (soluble fms-like tyrosine kinase-1, placental growth factor) and markers of endothelial activation (von Willebrand factor antigen), endothelial injury (fibronectin) and trophoblast debris (cell-free fetal DNA) were also determined. Plasma levels of ficolin-2 were significantly lower in healthy pregnant than in healthy non-pregnant women, while ficolin-3 levels did not differ significantly between the two groups. Furthermore, pre-eclamptic patients had significantly lower ficolin-2 and ficolin-3 concentrations than healthy non-pregnant and pregnant women. In the pre-eclamptic group, plasma ficolin-2 levels showed a significant positive correlation with serum placental growth factor (PlGF) concentrations and significant inverse correlations with serum levels of soluble fms-like tyrosine kinase-1 (sFlt-1), blood urea nitrogen and creatinine, serum lactate dehydrogenase activities, as well as with plasma VWF:antigen, fibronectin and cell-free fetal DNA concentrations. 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.
First Department of Obstetrics and Gynecology, Semmelweis University, Hungarian Academy of Sciences, Budapest, Hungary.
A
A
Halmos
J
J
Rigó
J
J
Szijártó
G
G
Füst
Z
Z
Prohászka
A
A
Molvarec
D000328:Adult; D015415:Biomarkers / Q000097:blood; D001806:Blood Urea Nitrogen; D016022:Case-Control Studies; D003167:Complement Activation; D003404:Creatinine / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005353:Fibronectins / Q000097:blood; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D037102:Lectins / Q000097:blood*; D018384:Oxidative Stress; D010920:Placenta / Q000378:metabolism; D000072483:Placenta Growth Factor; D011225:Pre-Eclampsia / Q000097:blood* / Q000276:immunology; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000097:blood; D014327:Trophoblasts / Q000378:metabolism; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis; D000097604:Ficolins
D015415:Biomarkers; D003404:Creatinine; D005353:Fibronectins; D006023:Glycoproteins; D037102:Lectins; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins; D040281:Vascular Endothelial Growth Factor Receptor-1; D014841:von Willebrand Factor; D000097604:Ficolins; C109662:FCN3 protein, human; C000608036:PGF protein, human