Authors
Pilkevich N. B.
Doctor of Medicine, Professor, Chair for Pathology1
Markovskaya V. A.
PhD (Biology), Head, Chair for Pathology1
Yavorskaya O. V.
Lecturer, Medical College1
Khabibullin R. R.
Senior Lecturer, Chair for Human Anatomy and Histology1; Head, Pathological Department of Immunohistochemistry2
Smirnova A. P.
Student1
1 - Belgorod State National Research University, Belgorod, Russian Federation
2 - Belgorod Pathoanatomical Bureau, Belgorod, Russian Federation
Corresponding Author
Pilkevich N. B.; e-mail: pilkevich@bsu.edu.ru
Conflict of interest
None declared.
Funding
The study had no sponsorship.
Abstract
Aim of the study. To analyze publications of scientific studies devoted to the study of biochemical and immunological aspects of the pathophysiology of acute respiratory distress syndrome. Material and methods. An analysis of 54 sources was conducted. The search for articles was carried out in the abstract databases Scopus and Web of Science, as well as in the search engines PubMed, eLIBRARY.RU and Google Scholar, from 2000 to December 2023. Conclusions. The immunological aspect of the pathophysiology of acute respiratory distress syndrome is characterized by the activation of the innate immune system and antigen-presenting cells, which contributes to the initiation of the immune response. In turn, neutrophils release cytotoxic molecules, active oxygen metabolites, bioactive lipids and proinflammatory cytokines and trigger an inflammatory cascade. Cytotoxic molecules cause tissue necrosis, initiate apoptosis and autophagy, which maintains and enhances inflammatory reactions and lung injury, as well as the formation of a vicious circle. Damage to vascular endothelial cells initiates coagulation, promoting the activation of platelets and procoagulant cascades, which leads to the formation of microthrombi in the pulmonary microcirculatory network and fibrin deposition in the intraalveolar and interstitial compartments. The interaction of platelets and neutrophils at the site of endothelial injury is considered a humoral regulatory process. Uncontrolled immunothrombosis can cause concomitant tissue damage and contribute to organ dysfunction.
Key words
Biochemical and immunological aspects, pathophysiology, respiratory distress syndrome
DOI
References
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