Stem Cell Populations and Regenerative Potential in Chronic Inflammatory Lung Diseases

Several acute and chronic inflammatory pathologies of the lung are accompanied by structural modifications of airway mucosa that vary depending on the severity, duration and type of the disease. These morphological changes, that determine organ dysfunction, are not always reversible. Indeed, the cycle of injury and repair, influencing airway wall regeneration, may sometimes break off and an exacerbation of the pathology may occur. The mechanisms at the base of airway remodelling during inflammation have been widely studied and numerous evidences indicate that the molecular dialogue among the cells of the mucosa has an essential role in orchestrating cell differentiation and tissue repair. In this review, we revise old notions on pulmonary morphology at the light of some of the most recent discoveries concerning stem cell differentiation, tissue homeostasis and organ regeneration of the lung

Effects of antioxidants on CSE-induced cell death in human asthmatic primary bronchial epithelial cells

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