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The study discusses the relationship of thiol concentrations in intercellular fluid with the level of peripheral blood mononuclear cells (MNCs) components of mitogen-activated (MAPK) / stress-activated (SAPK) and JAK/STAT signaling pathways, and nuclear transcription factor NF-κB in community-acquired pneumonia (CAP) convalescents. The content and level of phosphorylation of JAK2 protein kinase, signal transducers and transcription activators STAT3, STAT5A, STAT6, NF-κB nuclear transcription factor inhibitor (IκBα), JNK, ERK stress-activated protein kinases, and the level of nuclear transcription factor NF-κB p50 subunit were determined by ELISA in MNCs. The results of the study indicate that the stage of CAP convalescence is characterized by a lack of antioxidant protection manifested by a decrease in the concentration of thiol-containing compounds in cell culture supernatants, on the background of which there is a decrease in the level of phosphorylation of JAK2 protein kinase, factors STAT3, STAT5, STAT6, JNK, which is also associated with an increase in the level of phosphorylation of ERK protein kinase. The analysis showed that the thiol status is characterized by a positive relationship with the activity of STAT5A, JNK, p50. The thiol level and ERK, as well as STAT3, was characterized by a negative relationship. Thus, the increase in the thiol level contributes to an increase in the activity of the transcription factor STAT5A and a decrease in the activity of the transcription factor STAT3 with a corresponding change in cell reactivity with respect to specific cytokines, as well as a specific effect on the differentiation of individual populations of immunocompetent cells.

THE RELATIONSHIP OF THIOL STATUS, AND COMPONENTS OF SIGNALING PATHWAYS THAT REGULATE INFLAMMATION IN CONVALESCENTS WITH COMMUNITY-ACQUIRED PNEUMONIA