[Monocytes of human blood as a target of Streptococcus pyogenes components].

AIM: Study the effect of components of destroyed streptococci on human blood monocyte functions related to processes of trans-endothelial migration in vitro. MATERIALS AND METHODS: Mononuclear leukocytes, isolated from blood of healthy donors, endothelial cells of EA.hy 926 line and supernatant of ultrasound disintegrated Streptococcus pyogenes (DSS) were the objects of the study. Evaluation of adhesion and monocyte migration, level of expression of adhesion molecules and phosphokinases on monocytes was carried out by flow cytometry using monoclonal antibodies. Cytokine concentration was determined by using standard commercial test systems in enzyme immunoassay. RESULTS: Under the effect of DSS, expression of adhesion molecules CD162 and CD11b, as well as phospho-p38 MAPK changed, IL-6 and IL-8 secretion induction took place. DSS caused enhancement of migration and adhesive activity of monocytes, however, inhibited intensity of trans-endothelial migration. CONCLUSION: Products of destroyed streptococci have a multi-directional effect on human blood monocytes, that could be explained by the presence of components with varying biological activity in DSS.

[CD14++CD16- and CD14+CD16+ human monocytes adhesion to endothelial cells].

Two subsets of monocytes were identified in humans and other mammals blood based on different levels of CD14 and CD16 expression. These subsets have different patterns of adhesion molecules and chemokine receptors, which suggest different modes of interaction with endothelium and tissue traffic. Here, we investigated the ability of CD14+CD16+ and CD14++CD16- monocytes to adhesion to endothelial cells monolayer in presence and in the absence of pro- and anti-inflammatory cytokines. We demonstrated that CD14+CD16+ monocytes had higher level of adhesion to intact endothelial cells monolayer than CD14++CD16- monocytes. Significant increase in adhesion of CD14++CD16- and CD14+CD16+ monocytes subpopulations was observed in the presence of both TNF alpha and TNF alpha combinations with other cytokines. IFN gamma and IL-4 showed no independent effects on adhesion of monocytes. These results have demonstrated that both CD14++CD16- and CD14+CD16+ monocytes can be recruited to inflamed endothelium, but, in the absence of inflammation, CD14+CD16+ monocytes adhere to endothelial cells two times stronger than CD14++CD16- monocytes.