APOPTOSIS OF PERIPHERAL BLOOD LYMPHOCYTES AT BRONCHIAL ASTHMA OF A DIFFERENT SEVERITY DEGREE

Research objective: to study the features of realization of apoptosis of lymphocytes in the peripheral blood in patients with bronchial asthma of different severity in the period of exacerbation and out of it. 136 patients were divided into 2 groups depending on the severity of the disease. In the first group 67 patients with moderate bronchial asthma were included; the second group consisted of 69 patients with severe bronchial asthma among whom 31 patients constantly took systemic glucocorticosteroids. Spontaneous and Dexamethasone-induced apoptosis of lymphocytes in peripheral blood as well as the influence of the blocker of calcium channels on the modulator-induced programmable cellular death in the period of exacerbation of the disease and out of it were studied. It was found out that at bronchial asthma Dexamethasone-induced apoptosis has some features. The intensification of modulator-induced apoptosis at bronchial asthma of different severity in the conditions in vitro was revealed. But the serious course of the disease is characterized by the depression of apoptotic activity in lymphocytes, which proves an inflammation persistence in respiratory tracts and the intensification of immunocompetent cells survival. Thus, the existence of long existing immunocompetent cells in respiratory tracts is caused not only by their increased migration in the tissue, but also by the retardation of cells elimination owing to the disturbance of the processes of programmable cellular death, which is more accurately traced with the disease severity. It was found out that the suppression of the mechanism of calcium entering the cells via calcium channels of L-type of lymphocytes cytoplasmatic membrane has no impact on apoptosis-inducing effect of in vitro Dexamethasone. It was established that anti-apoptotic action of calcium channels blocker is completely lost in the period of bronchial asthma exacerbation.

бронхиальная астма, апоптоз, глюкокортикостероиды, bronchial asthma, apoptosis, glucocorticosteroids

1. Роль процессов клеточной гибели в развитии воспаления при бронхиальной астме / В.А.Невзорова [и др.] // Тихоокеанский мед. журн. 2006. №2. С.54–58.

2. Скибо Ю.В., Курмаева Н.Ш. Особенности апоптоза лимфоцитов у больных легкой и тяжелой атопической бронхиальной астмой // Практическая медицина. 2012. №61. С.62–68.

3. Global Initiative for Asthma (GINA). Global strategy for asthma management and prevention. 2011. URL: http://www.ginasthma.org

4. Mitochondrial Ca(2+) and apoptosis / C.Giorgi [et al.] // Cell Calcium. 2012. Vol.52, №1. Р.36–43.

5. Lymphocyte calcium signaling involves dihydropyridine-sensitive L-type calcium channels: facts and controversies / В.Gomes [et al.] // Crit. Rev. Immunol. 2004. Vol.24, №6. Р.425–447.

6. Jeong S.Y., Seol D.W. The role of mitochondria in apoptosis // BMB Rep. 2008. Vol.41, №1. P.11–22.

7. Effect of verapamil on bronchial goblet cells of asthma: an experimental study on sensitized animals / M.R.Khakzad [et al.] // Pulm. Pharmacol. Ther. 2012. Vol.25, №2. Р.163–168.

8. Pelletier L., Guéry J.C. Dihydropyridine receptor blockade in the treatment of asthma // Recent Pat. Inflamm. Allergy Drug Discov. 2008. Vol.2, №2. Р.109–116.

9. Schlossmacher G., Stevens A., White A. Glucocorticoid receptor-mediated apoptosis: mechanisms of resistance in cancer cells // J. Endocrinol. 2011. №1. P.17–25.

10. Apoptosis and airway inflammation in asthma / A.M.Vignola [et al.] // Apoptosis. 2000. Vol.5, №5. P.473–485.

11. New evidence of inflammation in asthma / A.M.Vignola [et al.] // Thorax. 2000. Vol.55, Suppl.2. P.59–60.