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

Abstract

The study discusses the relationship of thiol concentrations in intercellular fluid with the level of peripheral blood mononuclear cells (MNCs) in convalescents with community-acquired pneumonia (CAP) components MAPK/SAPK and JAK/STAT-signaling pathways, nuclear transcription factor NF-KB. The content and level of phosphorylation of JAK2 protein kinase, signal transducers and transcription activators STAT3, STAT5A, STAT6, NFKB nuclear transcription factor inhibitor (IkBa), stress-activated protein kinases JNK, ERK, the level of the p50 subunit of nuclear transcription factor NF-κB were determined by enzyme immunoassay in MNC. The results of the study indicate that the stage of reconvalescence of CAP is characterized by a lack of antioxidant protection, manifested by a decrease in the concentration of thiol compounds in the supernatant against which there is a decrease in the level of phosphorylation of protein kinase JAK2, factors STAT3, STAT5, STAT6, JNK, which is also associated with an increase in the level of phosphorylation of protein kinase ERK. The analysis showed that the thiol status is characterized by a positive relationship with the activity of STAT5A, JNK, p50. The level of thiols and ERK, as well as STAT3, was characterized by a negative relationship. Thus, the increase in the level of thiols contributes to the increase in the activity of the transcription factor STAT5A and decrease-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.

Keywords

• thiols
• stat5a
• pneumonia
• nf-kb