The link between cigarette smoke (CS) and lung inflammation is quite strong, however
relatively little is still known on the effects of CS on human bronchial epithelial cells
survival during asthma. In this study we focused our attention on the apoptotic effects
of CS on healthy (HC) and asthmatic (AS) primary bronchial epithelial cells (PBEC) and
on 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 were
obtained by bronchoscopy. PBEC were treated with oxidants (H2O), anti-oxidants (GSH
and AA) and cigarette smoke extracts (CSE). Early apoptosis (EA) and necrosis were
measured by flow cytometry using Annexin-V and propidium iodide.
After treatment with CSE 20%, AS showed an increased susceptibility to the CSE
treatment compared to HC (24.34+/-9.61 vs 48.45+/-11.91, p=0.003). Similarly, when EA
was taken into consideration, there was a significant increase of EA cells in the AS group
treated 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 instead
was able to protect significantly both HS and AS from CSE-induced cell death. In
particular, the association between GSH and CSE 20% determined a significant (p=0.005
in HC and p=0.003 in AS) increase of viability when compared to CSE alone and at the
same time EA levels dropped considerably (p<0.05 in HC and p=0.003 in AS) down in
the presence of this antioxidant Moreover, GSH treatment determined a significantly
bigger (p=0.002) overall increase in viability in the AS group when compared to the HC
group.
In view of this data it could be possible to hypothesise that the typical imbalance in
oxidants-antioxidants levels of asthmatic bronchial epithelial cells might be responsible
for their increased susceptibility to oxidative stress
