Effects of cigarette smoke extract (CSE) and lipopolysaccharide (LPS) on airway epithelial cells: a proteomic approach

Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by a progressive and largely irreversible airflow obstruction, which involves structural changes of the lung, including emphysema and small airway remodelling (1). Tobacco smoke exposure and recurrent infections of the airways play a crucial role in the progression of the disease and in the decline of respiratory function (2,3). Airway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Chronic inflammation of the airways plays a crucial role in the airway remodelling, in fact, it leads to the release of profibrotic cytokines and growth factors, which are linked to a repair and remodelling process that thickens the airway wall and narrows the airway lumen (4). We aimed to dissect the molecular mechanisms by which cigarette smoke extracts (CSE) and LPS, a constituent of the outer wall of gram-negative bacteria, may modulate the activation of airway epithelial cells, using a proteomic approach. Therefore, the immortalized normal bronchial epithelial cell line (16-HBE) were stimulated with CSE (10% and 20%) and LPS (1 ?g/ml), alone and/or in combination, for 24 hours. The extracted proteins were resolved by two-dimensional gel electrophoresis. Silver staining revealed modified expression of diverse spots (n.18) at the different experimental points. It is interesting, that some of these spots (n.6) seem to be modulated by the synergic action of CSE and LPS. These preliminary results could provide new information on the profile of activated airway epithelial cells upon CSE and LPS exposure.