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Features of TRPV1 and TRPV4 channels expression on subpopulations of peripheral blood monocytes in patients with COPD

https://doi.org/10.36604/1998-5029-2024-94-80-86

Abstract

Introduction. Chronic Obstructive Pulmonary Disease (COPD) is a widespread heterogeneous disease, with smoking and exposure to air pollutants being the main etiological factors. Monocytes and macrophages are among the most important cells involved in the pathogenesis of COPD. It has been established that TRP channels can be activated in response to cigarette smoke in models of respiratory diseases. Previously, we identified the influence of TRP channels on the progression of bronchial obstruction and the peculiarities of their expression on peripheral blood leukocytes in patients with COPD. Aim. To study the features of TRPV1 and TRPV4 channels expression on subpopulations of peripheral blood monocytes in patients with COPD. Materials and methods. The study included 47 patients with COPD of varying severity and 25 individuals in the control group. Monocytes subpopulations and the expression of TRPV1 and TRPV4 receptors were determined by flow cytometry. Results. The TRPV1 channels had higher expression on monocytes of COPD patients (99.1 [98.6–99.6]% vs. 97.7 [95.6–99.5]%, p = 0.07). Analysis of monocyte subpopulations revealed that TRPV1 expression was increased on non-classical monocytes of COPD patients (94.5 [91.5–97.2] vs. 88.0 [71.5–95.1], p = 0.04). An increase in TRPV1 and TRPV4 expression on non-classical monocytes was associated with a decrease in the number of CD115 receptors on these cells. Correlations between TRPV1 and CD115 expression, expressed as a percentage, were ρ = -0.31, p = 0.07. Correlations for the TRPV4 channel with CD115 expression were ρ = -0.31, p = 0.08. An increased CD116/CD115 ratio on non-classical monocytes was also accompanied by a rise in TRPV1 channels expression on these cells (ρ = 0.35, p = 0.04). Conclusion. The study established that COPD patients, as compared to the control group, exhibit higher TRPV1 expression on non-classical monocytes. It was also determined that increased expression of TRPV1 and TRPV4 is associated with the formation of a pro-inflammatory phenotype of monocytes.

About the Authors

D. A. Gassan
Far Eastern Scientific Center of Physiology and Pathology of Respiration
Russian Federation

Dina A. Gassan, PhD (Med.), Head of Laboratory of Mechanisms of Virus-Associated Developmental Pathologies

22 Kalinina Str., Blagoveshchensk, 675000



D. E. Naumov
Far Eastern Scientific Center of Physiology and Pathology of Respiration
Russian Federation

Denis E. Naumov, PhD (Med.), Head of Laboratory of Molecular and Translational Research

22 Kalinina Str., Blagoveshchensk, 675000



I. Yu. Sugaylo
Far Eastern Scientific Center of Physiology and Pathology of Respiration
Russian Federation

Ivana Yu. Sugaylo, PhD (Med.), Staff Scientist, Laboratory of Molecular and Translational Research

22 Kalinina Str., Blagoveshchensk, 675000



O. O. Kotova
Far Eastern Scientific Center of Physiology and Pathology of Respiration
Russian Federation

Olesya O. Kotova, PhD (Med.), Senior Staff Scientist, Laboratory of Mechanisms of Virus-Associated Developmental Pathologies

22 Kalinina Str., Blagoveshchensk, 675000



T. A. Maltseva
Far Eastern Scientific Center of Physiology and Pathology of Respiration
Russian Federation

Tatiana А. Maltseva, PhD (Med.), Staff Scientist, Laboratory of Molecular and Translational Research

22 Kalinina Str., Blagoveshchensk, 675000



V. P. Kolosov
Far Eastern Scientific Center of Physiology and Pathology of Respiration
Russian Federation

Victor P. Kolosov, MD, PhD, DSc (Med.), Academician of RAS, Professor, Scientific Director

22 Kalinina Str., Blagoveshchensk, 675000



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Gassan D.A., Naumov D.E., Sugaylo I.Yu., Kotova O.O., Maltseva T.A., Kolosov V.P. Features of TRPV1 and TRPV4 channels expression on subpopulations of peripheral blood monocytes in patients with COPD. Bulletin Physiology and Pathology of Respiration. 2024;(94):80-86. (In Russ.) https://doi.org/10.36604/1998-5029-2024-94-80-86

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ISSN 1998-5029 (Print)