THE EFFECT OF HEAT SHOCK PROTEIN HSP70 ON THE MECHANISMS OF CELLULAR RESPONSES OF BLOODPHAGOCYTES AT THE ACTIONOF LIPOPOLYSACCHARIDES
Lipopolysaccharides (LPS) play an important role in the pathogenesis of gram-negative sepsis and other diseases. The cells of innate immune, including blood phagocytes, playan important role in these pathologies. Interaction of LPS and TLR4 of phagocytes leads to activation of intracellular signaling pathways of the cell-target of LPS and the subsequent cellular response, which is characterized increasing production of reactive oxygen species (ROS) and the synthesis of proinflammatory cytokines. Synthesis and secretion of heat shock protein (HSP70)are increased at the sepsis and other inflammatory diseases. The goal of this study was to investigate the effect of exogenousHSP70 on intracellular signaling pathwaysinvolved in the generation of ROS at the action of LPS. It is shown that phospholipase C (PLC), phosphatidylinositol 3 kinase (PI3K), extracellular signal – regulated kinase (ERK), p38 MAPK are involved in the mechanism of the HSP70 action on human neutrophils and monocytes.