pulmoПульмонологияPULMONOLOGIYA0869-01892541-9617Scientific and Practical Journal “PULMONOLOGIYA” LLCpulmo-2731Research ArticleОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯORIGINAL STUDIESМеханизмы дексаметазон-индуцированного апоптоза лимфоцитов при ато­пической бронхиальной астмеMechanisms of dexametazone-induced apoptosis of lymphocytes in atopic bronchial asthmaБойчукС. В.BoichukS. V.

Кафедра патофизиологии

Кафедра аллергологии

МустафинИ. Г.MustafinI. S.

Кафедра патофизиологии

Кафедра аллергологии

ФассаховР. С.FassakhovR. S.

Кафедра патофизиологии

Кафедра аллергологии

Казанский государственный медицинский университет; Республиканский Центр по борьбе со СПИДом Минздрава РТ; Казанская государственная медицинская академияRussian Federation200325092021021016Copyright © Бойчук С.В., Мустафин И.Г., Фассахов Р.С., 20212021Бойчук С.В., Мустафин И.Г., Фассахов Р.С.Boichuk S.V., Mustafin I.S., Fassakhov R.S.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.pulmonology.ru/pulm/article/view/2731

Изучали механизмы спонтанного апоптоза лимфоцитов (Лф) периферической крови доноров и больных атопической бронхиальной астмой (АБА), а также апоптоза, индуцированного дексаметазоном (Дн) и ионофором Са2+. В качестве маркеров апоптоза Лф использовали динамику изменения величины митохондриального потенциала (МП), уровня экспрессии фосфатидилсерина (ФС), параметров прямого и бокового светорассеивания, а также фрагментации ДНК. Изучаемые параметры апоптоза оценивали методом проточной цитофлюорометрии. У Лф больных АБА при инкубации в среде фрагментации ДНК наблюдается в меньшей степени и на более поздних сроках по сравнению с контролем. Различий в остальных изучаемых показателях апоптоза Лф между исследуемыми группами не выявлено. Дн индуцирует фрагментацию ДНК у Лф больных АБА на более ранних сроках и в большей степени при 72, 96 и 120 ч инкубации по сравнению с контролем. Инкубация Лф больных АБА с Дн приводила к значительному снижению их МП по сравнению с контролем, начиная с 48 ч инкубации. Дн-индуцированное снижение МП коррелирует с повышением уровня экспрессии ФС. Аналогичные результаты получены при апоптозе Лф, индуцированном ионофором Са2+. Результаты свидетельствуют об устойчивости Лф больных АБА к спонтанному апоптозу. Дн-индуцированный апоптоз Лф является митохондрий-опосредованным, а чувствительность Лф больных АБА к Дн-индуцированному апоптозу может быть обусловлена значительными (по сравнению с контролем) изменениями величины их МП.

Study results of spontaneous and dexamethazone (DEX)-induced or Ca2+ ionophor-induced apoptosis of peripheral blood lymphocytes (PBL) in healthy donors and atopic asthma (BA) patients are shown at the pre­sent work. The apoptosis was evaluated by several parameters: change in mitochondrial potential (MP), a ievel of phosphatidylserine (PS) expression on the outer leaflet of the cell membrane, forward (FSC) and side scat­ter (SSC) parameters and DNA fragmentation using flow cytometry. PBL of BA patients incubated in a culture showed later and less intensive DNA fragmentation in comparison with the controls. There were no differences between spontaneous MP and PS dynamics between the study groups. The DEX induced DNA fragmentation significantly earlier and greater after 72, 96 and 120 hrs of the incubation in the BA patients than in the con­trols. PBL incubation with DEX in the BA patients showed a significant decrease in the MP after 48 hrs of the incubation and later compared with the donors. The DEX-induced MP reduction correlated with the increase in the PS expression level. The analogous results were obtained for the Ca2+ ionophor-induced apoptosis. They demonstrated the resistance of PBL to spontaneous apoptosis in BA patients. The DEX-induced apoptosis of PBL was mitochondria-dependent. The PBL sensitivity to the DEX-induced apoptosis in the BA patients may be provided by their MP significant shifts compared with the controls.

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The authors declare that there are no conflicts of interest present.