Autor: |
Elisabetta Pace, Maria Ferraro, Marta Ida Minervini, Patrizio Vitulo, Loredana Pipitone, Giuseppina Chiappara, Liboria Siena, Angela Marina Montalbano, Malcolm Johnson, Mark Gjomarkaj |
Jazyk: |
angličtina |
Rok vydání: |
2012 |
Předmět: |
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Zdroj: |
PLoS ONE, Vol 7, Iss 3, p e33601 (2012) |
Druh dokumentu: |
article |
ISSN: |
1932-6203 |
DOI: |
10.1371/journal.pone.0033601 |
Popis: |
BACKGROUND: Altered 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. METHODS: The 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). RESULTS: In 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. CONCLUSIONS: This study provides new insights on the possible mechanisms involved in the alteration of innate immunity mechanisms in COPD. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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