The link between cigarette smoke (CS) and lung inflammation is quite strong, howeverrelatively little is still known on the effects of CS on human bronchial epithelial cellssurvival during asthma. In this study we focused our attention on the apoptotic effectsof CS on healthy (HC) and asthmatic (AS) primary bronchial epithelial cells (PBEC) andon the role of antioxidants to protect epithelial cells from CSE-induced apoptosis.Twenty subjects (10 HC and 10 AS) were recruited for this study and PBEC wereobtained by bronchoscopy. PBEC were treated with oxidants (H2O), anti-oxidants (GSHand AA) and cigarette smoke extracts (CSE). Early apoptosis (EA) and necrosis weremeasured by flow cytometry using Annexin-V and propidium iodide.After treatment with CSE 20%, AS showed an increased susceptibility to the CSEtreatment compared to HC (24.34+/-9.61 vs 48.45+/-11.91, p=0.003). Similarly, when EAwas taken into consideration, there was a significant increase of EA cells in the AS grouptreated with CSE compared to HC (33.12+/-10.38 vs 16.73+/-6.92, p<0.05).AA failed to protect both HS and AS PBEC from CSE-induced cell death. GSH insteadwas able to protect significantly both HS and AS from CSE-induced cell death. Inparticular, the association between GSH and CSE 20% determined a significant (p=0.005in HC and p=0.003 in AS) increase of viability when compared to CSE alone and at thesame time EA levels dropped considerably (p<0.05 in HC and p=0.003 in AS) down inthe presence of this antioxidant Moreover, GSH treatment determined a significantlybigger (p=0.002) overall increase in viability in the AS group when compared to the HCgroup.In view of this data it could be possible to hypothesise that the typical imbalance inoxidants-antioxidants levels of asthmatic bronchial epithelial cells might be responsiblefor their increased susceptibility to oxidative stress.
|Number of pages||0|
|Publication status||Published - 2010|