PLATELET-MONOCYTE COMPLEXES AND THEIR POTENTIAL ROLE IN THE PATHOGENESIS OF PREECLAMPSIA

Abstract. Pregnancy represents the state with particularly activated constituents of hemostasis and immune systems. Hyperactivation of platelets and monocytes may be a causative factor for pregnancy complications including preeclampsia. The pathogenetic role of platelet-monocyte complexes (PMC), recognized as diagnostic marker and therapeutic target, is poorly investigated. The aim of the study was to determine quantitative changes in the peripheral blood PMC level and antigenic phenotype in preeclampsia, and to evaluate effects of platelets on the expression of monocyte surface marker proteins in normal and pathological pregnancy. The tested groups included third trimester pregnant women diagnosed with severe preeclampsia (35-41 weeks of gestation) and women with uncomplicated (physiological) pregnancies (33-41 weeks of gestation). All participants were between the age of 24 and 42 years. PMC levels and CD62P, CD11b, CD86, CD162, HLA-DR, TREM-1 expressed by PMC and free circulating cells were determined by flow cytometry in the peripheral blood total monocytes and monocyte subpopulations.It was found that PMC level increased (29.2% of total monocyte population) when compared to uncomplicated pregnancy (17.5%), and this augmentation was ensured by two PMC-forming monocyte subpopulations: classical and intermediate. Moreover, expression levels of platelet and monocyte activation markers CD62P, CD162, HLA-DR, CD86, TREM-1, CD11b were significantly higher in preeclampsia. The fractions of classical, intermediate and non-classical monocytes differently contributed to preeclampsia-associated changes in the expression levels of monocyte activation markers. Comparison of PMC and free circulating monocytes demonstrated that observed changes in the surface antigenic phenotype of monocytes within PMC were ensured by platelets and other factors. In preeclampsia, platelet-induced augmentation of monocyte inflammatory and adhesive capacities displayed itself in the increased TREM-1 and CD11b expression. In contrast, increased levels of HLA-DR and CD86 in monocytes were not induced by the interaction with platelets. The results of the study suggest that preeclampsia is accompanied by increased peripheral blood PMC levels and activation of monocytes within PMC, demonstrate immunomodulatory effect of platelets, and provide a rationale for the evaluation of expression patterns of PMC surface antigenic markers with diagnostic and therapeutic purposes.

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