Analysis of the Expression of Key Protein Regulators of Apoptosis and Autophagy in T-Lymphocytes of Patients with Bronchial Asthma

Bronchial asthma is a disease characterized by T-lymphocyte resistance to apoptosis. Recent studies have shown that there is an alternative form of cell death - autophagy. Since apoptosis in T-cells of patients with asthma is reduced, we suggested that autophagy could be initiated. The aim of the study is to perform a comparative analysis of the expression of apoptosis and autophagy key proteins in Tlymphocytes of patients with mild and severe bronchial asthma. To achieve this aim, the Western blot method was applied. The results were processed with the help of R statistics. Boxsplots were used to present the data. We showed that in the group with mild asthma the amount of caspase-3 increases during cultivation (spontaneous apoptosis is activated). In the group with the severe form, its content did not change. Autophagy activation was assessed by the presence of LC3-II protein. The results showed that form II of LC3-protein is present only in the group with the severe form. Therefore, the analysis of the content of key proteins of autophagy - Rubicon and UVRAG - in the cells of this category of patients was carried out and a significantly increased expression of these proteins was detected. In addition, we found a significant increase of UVRAG compared with Rubicon. Thus, inhibition of apoptosis is characteristic of T-lymphocytes of patients with bronchial asthma. However, in the mild group, a decrease of nutrients in the culture medium stimulated the launch of apoptosis, which was manifested in an increase in the content of caspase-3 and a decrease in Bcl-2. In the severe group, cell cultivation did not cause an increase in apoptotic activity, autophagy was activated instead, and we assume that for this group of patients it is an alternative way of cell death.