COMPARATIVE CHARACTERISTICS OF FATTY ACID COMPOSITION OF BLOOD PLASMA AND ERYTHROCYTES IN CHRONIC RESPIRATORY DISEASES

Abstract

Background and Aims: Chronic inflammation is a key mechanism for the development of asthma-COPD overlap syndrome. Disruption of immune processes is associated with changes in the metabolism of n-3 and n-6 polyunsaturated fatty acids (PUFA), the synthesis of proinflammatory lipid mediators (leukotrienes, thromboxanes) and specialized pro-resolving mediators (SPM). However, there is insufficient data on the role of impaired fatty acid metabolism of immune cells in the development of asthma-COPD overlap syndrome. The aim is to study the composition and metabolic transformations of PUFA in leukocytes and the level of eicosanoids in asthma-COPD overlap syndrome. Methods: Levels were quantified in leukocytes from 126 human volunteers by LC / MS. The level of thromboxane B2 and leukotriene B4 was studied by ELISA (Amersham Biosciences). Immunological examination was performed on a BD FACS Canto II cytofluometer. Results: A decrease in the level of 18: 2n-6, 20: 3n-6, 20: 4n-6, 22: 4n-6 and 20: 5n-3, 22: 6n-3 in leukocytes was detected against the background of an increase in the synthesis of thromboxane B2 and leukotriene B4 in patients with asthma-COPD overlap syndrome. On the one hand, a decrease in the level of n-6 PUFA indicates a decrease in the activity of the Δ5 and Δ6 enzymes of desaturase and elongase, on the other hand, on their active use in the synthesis of pro-inflammatory eicosanoids. This fact was confirmed by a high level of thromboxane B2 and leukotriene B4 in the serum. A deficiency of 20: 5n-3, 22: 6n-3 in the leukocyte membrane indicates an inhibition of SPM synthesis. Conclusions: Thus, impaired metabolism of PUFA in leukocytes provokes the development of chronic inflammation in asthma-COPD overlap syndrome.