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Aim: To evaluate diagnostic value of lipopolysaccharide-binding protein (LBP) level in different infectious processes and dysbiosis., Materials and Methods: Serum samples of patients with salmonellosis, urogenital chlamydiosis, community-acquired pneumonia, polypous rhinosinusitis, and bacterial vaginosis were studied., Results: LBP level were lower in patients with salmonellosis compared to healthy persons and decreased with increasing severity of the disease. Higher levels of LBP were detected in patients with chlamydiosis. Direct correlation between LBP level and etiology and severity of community-acquired pneumonia was demonstrated. In patients with polypous sinusitis, LBP level correlated directly with duration of disease, and inversely--with duration of remission. Twofold increase of mean LBP blood concentration and its correlation with duration of dysbiosis in patients with bacterial vaginosis were revealed., Conclusion: Multidirectional modulation of antiendotoxin defense was observed in different pathological conditions.

The present paper shows that murine serum nuclease activity increases following P.berghei infection. DNA activity begins increasing just 48 hours after infection. Following 78 hours, it achieves the maximum, by exceeding the baseline level by 6 times. Then DNA activity starts decreasing and following 94 hours after infection it is just thrice higher than the baseline. Serum RNA activity shows only 30% increases 72 hours after infection and returns to the baseline following 94 hours. Microscopic monitoring indicates that only single malaria causative agents appear in the red blood cells in this period. The peak increases in nuclease activities after P.berghei infection are assumed to be associated with the induction of serum infection.

Depending on the type of autonomous regulation, differences in basic levels of interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha) were revealed under conditions of hyperthermia in healthy subjects aged 19-21. A parasympathetic type of autonomous regulation corresponded to higher initial levels of proinflammatory cytokinesis, whereas a dominating sympathetic type corresponded to lower levels of the IL-1 beta and TNF alpha. The subjects with the latter type of regulation revealed an increase in the IL-1 beta TNF alpha combined with a higher heat tolerance. The subjects with the former type of regulation revealed a lower heat tolerance. The increase in the alpha2-macroglobulin appeared to be a most typical acute phase response of the human body to hyperthermia.

Role of acute phase proteins (APP) and mechanisms that regulate their synthesis in the liver are considered. It is known that acute infection, trauma and neoplastic growth cause the acute phase response characterized by a complex of local and systemic reactions of the organism. Production of some acute phase plasma proteins increases (positive APP) while concentration of the others decreases (negative APP). In this review the role of the most important positive APP, such as C-reactive protein, the third component of the complement, alpha 1-antitrypsin, serum amyloid haptoglobin, hemopexin and some others and of negative APP such as albumin, transferrin, apoliprotein A-1 is discussed. Synthesis of APP in hepatocytes is regulated by three main inflammatory cytokines, such as IL-1, IL-6, TNF, produced mainly by immunocompetent cells, and by glucocorticoids. Peculiarities of each cytokine effect, their interaction during APP synthesis as well as their regulation by receptors-antagonists and by autoantibodies are discussed. The data described provide evidence for the close relation which exists between the immune system and the liver and is required to maintain homeostasis.

Process of proteins' modification under pathology are considered and classified. Attention is focused on the processes of postsynthetic modification. It is suggested not only proteins with the structure different from that in the norm to be considered as defective but also those whose biosynthesis does not provide the fulfilment of a definite function by them. Processes of proteins damaging by certain metabolites and xenobiotics are considered in detail. It is shown that all proteins of the organism may be damaged both by the excess of the natural metabolite (glucose) and by xenobiotics. The hypothesis is advanced on the important role of albumin as a primary barrier in the organism response on the chemical affection. The cooperative mechanism of the ligands' binding which underlies the detoxication function of the albumin is postulated.