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research
Beta defensin-2 is reduced in central but not in distal airways of smoker COPD patients
Authors
A Aderem
A Biragyn
+50 more
A Bruno
A Busacker
A Kato
AL Cozens
Angela Marina Montalbano
C Herr
CJ Murray
CY Kao
D Droemann
D Miotto
Dominik Hartl
E Doz
E Pace
E Pace
E Pace
E Pace
E Pace
Elisabetta Pace
F Niyonsaba
G Chiappara
Giuseppina Chiappara
J Pons
JC Hogg
JL Curtis
JL Imler
K Fellerman
K Kolble
L Petecchia
Liboria Siena
LM Hamilton
Loredana Pipitone
M Saetta
Malcolm Johnson
Maria Ferraro
Mark Gjomarkaj
Marta Ida Minervini
MG Cosio
N Kanda
Patrizio Vitulo
Q Sha
R MacRedmond
R O'Donnell
S Boodoo
S Sethi
S Sethi
SD Sullivan
TS Lapperre
V Kim
W Zhang
X Zhang
Publication date
16 March 2012
Publisher
'Public Library of Science (PLoS)'
Doi
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on
PubMed
Abstract
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. © 2012 Pace et al
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