Apoptosis in blood lymphocytes in atopic bronchial asthma

Abstract

The present work shows results of investigation of spontaneous and induced apoptosis in blood lymphocytes (L) in healthy donors and atopic asthma (AA) patients. Apoptosis was assessed by several parameters: changes of the mitochondrial potential (MP) and of phosphatidylserine (PS) expression level on the outer leaflet plasma membrane, forward and side scatter parameters and DNA fragmentation using the flow cytometry. We obtained that the DNA fragmentation in the AA patients’ L incubated in a culture became later and less than in the donors. The delayed DNA fragmentation did not depend on the Mn²⁺-DNAase activity. Spontaneous and induced reduction in the MP and increase in the PS expression were the earliest apoptosis markers which inversely interrelated and were observed even in optically intact cells. Changes of these parameters preceded the DNA fragmentation. There were no differences in the spontaneous changes of the MP and the PS levels between two study groups. Thus, the recognition of the apoptotic L in AA was not injured and a necessary factor for the apoptotic L elimination was their DNA fragmentation. The incubation of the donors’ and AA patients’ L with Ca²⁺ ionophore A23187 induced the similar changes of the MP and the PS expression and the DNA fragmentation. So, the spontaneous and induced types of apoptosis have common mechanisms and are initiated with mitochondria involvement. The lymphocyte mitochondria are thought to be a universal integrator of apoptotic stimuli and the réduction in the MP is the earliest characteristic of the apoptosis inducing the following apoptotic features.