Exogenous heat shock protein HSP70 protects human blood phagocytes at the action of different chemotypes of lipopolysaccharide

392 It is known that lipopolysaccharides (LPS) play the key role in the development of Gram negative sepsis. They also have important implications for develop ment of certain socially significant diseases [1]. The majority of the enterobacterium Escherichia coli have S form of LPS, which includes hydrophobic lipid A, an oligosaccharide core, and O antigen. In addition to the LPS S form, enterobacteria also synthetize core defect molecules of LPS (R chemotypes), which have lipid A and a core part of different lengths. Core defect structures are marked Rb–Re chemotypes; and structures that have a complete external core, Ra chemotype [2]. Entering blood stream, LPS first inter act with lipopolysaccharide binding protein (LBP), then with CD14 receptor of target cells. After that, LPS are transferred from CD14 to MD 2 (lymphocyte antigen 96), and subsequent formation of two com plexes LPS MD 2 TLR4 occurs; then, they form a heterodimer receptor complex in the membrane of target cells [3]. Then, a signal is transferred from the receptor to transcription factors in target cells, and the cell response is developed. At the early stages of cell response, reactive oxygen species (ROS) production, as well as adhesion factors expression, increase. In a later period, pro inflammatory cytokines are synthe tized, TNF α being the first of them to be secreted [4].