Possible role of platelet-monocyte complexes in the pathogenesis of recurrent pregnancy loss

Recurrent pregnancy loss (RPL) is a significant clinical problem that affects 1-5% of population. Moreover, the cause of RPL remains unknown in more than half of cases. Possible reasons include imbalanced maternal hemostasis, thrombosis of uteroplacental vessels, decreased placental perfusion and hypoxia. Changes in morphofunctional features of monocytes and platelet-monocyte aggregates may be the factors causing pregnancy complications. However, role of platelet-monocyte complexes (PMC) in pathogenesis of RPL is unknown. The purpose of our study was to determine quantitative changes in contents and antigenic phenotype of PMCs in peripheral blood of the patients with RPL, and to assess the effect of platelets on the expression of monocyte surface proteins in normal and pathological pregnancy. The study groups consisted of 6 to12-week pregnant women diagnosed with RPL and females with uncomplicated pregnancy (7-12 weeks). PMC content and expression of CD62P, CD11b, CD86, CD162, HLA-DR, TREM-1 were determined in total cell population and subpopulations of peripheral blood monocytes using cytofluorimetry technique. It was found that PMC level was increased in patients with RPL (26.5%) compared to uncomplicated pregnancy (15.3%) with all monocyte subpopulations contributing to this increase. Decrease in HLA-DR expression and increase in CD11b expression was observed in total PMCs, while expression of CD62P, CD162, CD86 and TREM-1 did not change significantly. Monocyte subpopulations were differently involved into the RPLassociated expression of activation markers, while the changes detected in distinct subpopulations were not always evident in total monocyte populations in recurrent pregnancy loss. A comparison of PMC and free monocytes demonstrated that changes in surface phenotype of monocytes were caused by platelets and other exogenous factors. In patients with RPL, we observed platelet-induced increase in adhesive properties of monocytes which manifested as increased CD11b expression. In contrast, decrease in monocyte HLA-DR levels was not caused by platelets. The results obtained suggest that RPL is accompanied by increased level of peripheral blood PMC and changes in antigenic profile of platelet-associated and free monocytes, thus demonstrating the immunomodulatory effect of platelets, and also confirming the importance of determining expression patterns of surface antigenic markers of PMC for diagnostic and therapeutic purposes.

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