Source: Annual Congress 2002 - Cellular reactions in allergy in humans and animals
Disease area: Airway diseases

Abstract

The mechanisms of GC-induced peripheral blood lymphocyte (PBL) apoptosis obtained from donors and ABA patients were investigated. Various PBL populations were incubated with dexamethasone (DEX) and several apoptosis markers (transmembrane mitochondrial potential level (MP), out plasma membrane phosphatidylserine (PS) exposure, BcL-2 expression levels, DNA fragmentation, and number of Fas+ and FasL+-cells) were measured by flow cytometry method.
There were no differences between the number of MPlow, BcL-2+, PS+-cells obtained from freshly isolated PBL obtained from ABA and donors, but number of Fas+-PBL (CD4+- and CD8+-cells) significantly decreased in ABA patients. Number of Fas+-cells obtained from GC-treated ABA patients were lower that in untreated group of ABA. However DEX didn[scquote]t induce changes of quantities of Fas+ and FasL+-cells in vitro. Incubation of PBL with DEX dose- and time-dependently reduced levels of MP, BcL-2 expression, induced DNA fragmentation and increased number of PS+-cells, which was significantly higher in PBL obtained from ABA patients. CD4+-cells were more sensitive PBL population to apoptogenic action of DEX. Decrease of MP and BcL-2 were closely dependent and most early features of DEX-induced PBL apoptosis. Appearance of PS on PBL out plasma membrane reversibly depended to the MP level.
We conclude that PBL (especially CD4+) obtained from ABA were sensitive to DEX-induced apoptosis. One of GC targets may be mitochondrial membrane and BcL-2 protein level and sensitivity of PBL obtained from ABA to GC-induced apoptosis is dependent by significant influence to this antiapoptotic protein.

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Citations should be made in the following way:
S. V. Boichuk, I. G. Mustafin, R. S. Fassahov, D. Y. Tereshenko (Kazan, Russia). The mechanisms of glucocorticoid (GC)-induced lymphocyte apoptosis in atopic bronchial asthma (ABA). Eur Respir J 2002; 20: Suppl. 38, 305

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