Introduction . The pathogenesis of bronchial asthma largely depends on changes in the cells’ energy state, in which the mitochondrial membrane potential (MMP) plays a major role. A decrease in MMP is evident at the early stages of asthma development and may be one of the key pathological signs of the disease. The course and progression of asthma can be aggravated by various factors, including airborne particulate matter (PM). However, information on MMP changes in individual lymphocyte subpopulations under PM exposure is scarce. Aim . To establish disturbances in the mitochondrial membrane potential of CD4+ cells in patients with mild asthma under the influence of ground-level atmospheric particulate matter. Materials and methods . This in vitro study included 131 patients with asthma and 60 apparently healthy individuals. Model suspensions simulating the multicomponent pollution of Vladivostok air were used as a challenge. MMP levels (MMP-1 – MMP-5) were determined by flow cytometry, and the MMP coefficient (cMMP) was calculated. Results . In asthma the main shifts occurred at MMP-1, MMP-2 and MMP-3 levels: the proportion of cells with high MMP decreased, whereas that of cells with moderately reduced MMP (MMP-2 and MMP-3) increased. PM exposure induced significant redistribution of MMP levels in asthma patients. Lower disease control was associated with more pronounced energy disturbances: in controlled versus partially controlled asthma, cMMP was 82.9% lower. Under PM exposure, cMMP fell by 27.2% and 16.3% in controlled and partially controlled asthma, respectively, compared with unexposed groups. Conclusion . The study reveals features of CD4+-cell MMP impairment in mild bronchial asthma under atmospheric PM exposure, depending on disease-control level. Assessing MMP-level redistribution and the cMMP as an integral indicator of CD4+-cell energy status may facilitate early detection of energy-metabolism disorders in asthma and help optimise prevention of disease progression.
Elena V. Kondratyeva (Sun,) studied this question.