THE STATE OF THE CELLS OF THE IMMUNE SYSTEM IN EXPERIMENTAL IMMUNE-MEDIATED INFLAMMATION OF VARIOUS GENESIS

• Main Authors: S.I. Pavlovych, N.G. Grushka, O.A. Kondratska, N.O. Krasutska, R.I. Yanchii
• Format: Article
• Language: English
• Published: Bogomolets National Medical University 2021-06-01
• Series: Медична наука України
• Subjects: hyperimmunocomplexemia, endotoxemia, cells of the immune system, dna damage, cell death
• Online Access: https://msu-journal.com/index.php/journal/article/view/283
• ISSN: 2664-472X; 2664-4738

Relevance. Immune-mediated inflammation of various genesis plays a significant pathogenetic role in autoimmune, allergic, inflammatory and infectious diseases. The objective of the work was a comparative study of the functional status and pathways of cell death of natural and adaptive immunity in mice under the conditions of experimental hyperimmunocomplexemia and endotoxemia to identify the features and common cellular mechanisms of these pathologies. Materials and methods. Hyperimmunocomplexemia was simulated by six-fold immunization of female mice with increasing doses of the antigen, bovine serum albumin (BSA), once a week; the endotoxemia model was induced by the administration of lipopolysaccharide (LPS). Results. The use of both BSA and LPS led to a systemic inflammatory process with significant neutrophilia with a shift of the leukogram to the left. There was a significant increase in the functional and metabolic activity of nonspecific resistance cells. Genotoxic stress was observed in thymus cells and lymph nodes with significant DNA damage, decreased viability, and a significant increase in necrotic death. Violation of the plasma membrane integrity of primary alteration and the release of the cellular content outside has a strong pro-inflammatory and immunogenic effect, which can lead to further intensification of the disease and an increase in its duration with a tendency to chronicity of the pathological process. Conclusions. Thus, both models are characterized by the development of immune-inflammatory processes that lead to significant DNA damage and cell death, which can cause a new round of intensification of necrotic, inflammatory and autoimmune reactions in the body.