Abstract
Background: Osteopontin (OPN) has been associated with inflammation and fibrosis. OPN is increased in asthma and is related to the underlying severity and to features expressing remodeling and inflammation. Smoking may modify the inflammatory pattern of the airways.
Aims and objectives: To evaluate the levels of OPN in sputum supernatants of asthma patients and to investigate the possible role of smoking as well as associations with mediators and cells involved in the inflammatory and remodeling process.
Methods: We studied 98 asthma patients (51 smokers) and 40 healthy subjects (20 smokers) who underwent lung function tests, bronchial hyperresponsiveness to methacholine, and sputum induction for cell count identification and measurement of OPN, VEGF, TGF-β1, CysLTs, IL-13, ECP and IL-8 in supernatants. The concentrations of all mediators were measured using enzyme immunoassays.
Results: Median OPN levels (pg/ml) were significantly higher in smoking asthmatics (SA) compared to non-smoking asthmatics (NSA), and both smoking and non smoking controls [120 (651, 1793) vs 210 (120, 404) vs 50 (42, 70) vs 102 (71, 156) pg/ml, respectively; p<0.0001]. Regression analysis provided significant associations between log OPN and sputum neutrophils, IL-8, IL-13 and TGF-β1. The most significant association of TGF-β1 was the one with OPN. These associations were observed only in SA. No significant associations were observed between OPN, lung function tests and PD15 to methacholine in all groups.
Conclusions: OPN levels are affected by the smoking habit in asthma. The associations of OPN with sputum neutrophils, TGF-β1, IL-13 and IL-8, only in SA, suggest a possible role for OPN in the inflammatory and remodeling process in SA.
- © 2011 ERS
