• Elisabetta Pace, Maria Ferraro, Marta Ida Minervini, Patrizio Vitulo, Loredana Pipitone, Giuseppina Chiappara, Liboria Siena, Angela Marina Montalbano, Malcolm Johnson, and Mark Gjomarkaj.
• Institute of Biomedicine and Molecular Immunology, National Research Council, Palermo, Italy. pace@ibim.cnr.it
• Plos One. 2012 Jan 1; 7 (3): e33601.

BackgroundAltered pulmonary defenses in chronic obstructive pulmonary disease (COPD) may promote distal airways bacterial colonization. The expression/activation of Toll Like receptors (TLR) and beta 2 defensin (HBD2) release by epithelial cells crucially affect pulmonary defence mechanisms.MethodsThe epithelial expression of TLR4 and of HBD2 was assessed in surgical specimens from current smokers COPD (s-COPD; n = 17), ex-smokers COPD (ex-s-COPD; n = 8), smokers without COPD (S; n = 12), and from non-smoker non-COPD subjects (C; n = 13).ResultsIn distal airways, s-COPD highly expressed TLR4 and HBD2. In central airways, S and s-COPD showed increased TLR4 expression. Lower HBD2 expression was observed in central airways of s-COPD when compared to S and to ex-s-COPD. s-COPD had a reduced HBD2 gene expression as demonstrated by real-time PCR on micro-dissected bronchial epithelial cells. Furthermore, HBD2 expression positively correlated with FEV1/FVC ratio and inversely correlated with the cigarette smoke exposure. In a bronchial epithelial cell line (16 HBE) IL-1β significantly induced the HBD2 mRNA expression and cigarette smoke extracts significantly counteracted this IL-1 mediated effect reducing both the activation of NFkB pathway and the interaction between NFkB and HBD2 promoter.ConclusionsThis study provides new insights on the possible mechanisms involved in the alteration of innate immunity mechanisms in COPD.

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