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Beta defensin-2 is reduced in central but not in distal airways of smoker COPD patients

Pace, E and Ferraro, M and Minervini, MI and Vitulo, P and Pipitone, L and Chiappara, G and Siena, L and Montalbano, AM and Johnson, M and Gjomarkaj, M (2012) Beta defensin-2 is reduced in central but not in distal airways of smoker COPD patients. PLoS ONE, 7 (3).

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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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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Pace, E
Ferraro, M
Minervini, MImam419@pitt.eduMAM419
Vitulo, P
Pipitone, L
Chiappara, G
Siena, L
Montalbano, AM
Johnson, M
Gjomarkaj, M
Contributors:
ContributionContributors NameEmailPitt UsernameORCID
EditorHartl, DominikUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Date: 16 March 2012
Date Type: Publication
Journal or Publication Title: PLoS ONE
Volume: 7
Number: 3
DOI or Unique Handle: 10.1371/journal.pone.0033601
Schools and Programs: School of Medicine > Pathology
Refereed: Yes
MeSH Headings: Aged; Base Sequence; Bronchi--metabolism; Bronchi--pathology; Case-Control Studies; Cell Line; Down-Regulation; Epithelial Cells--metabolism; Epithelial Cells--pathology; Female; Humans; Immunohistochemistry; Male; Middle Aged; Pulmonary Disease, Chronic Obstructive--etiology; Pulmonary Disease, Chronic Obstructive--genetics; Pulmonary Disease, Chronic Obstructive--metabolism; Pulmonary Disease, Chronic Obstructive--pathology; RNA, Messenger--genetics; RNA, Messenger--metabolism; Real-Time Polymerase Chain Reaction; Smoking--adverse effects; Smoking--genetics; Smoking--metabolism; Toll-Like Receptor 4--metabolism; beta-Defensins--genetics; beta-Defensins--metabolism
Other ID: NLM PMC3306426
PubMed Central ID: PMC3306426
PubMed ID: 22438960
Date Deposited: 13 Sep 2012 20:23
Last Modified: 30 Jun 2018 22:55
URI: http://d-scholarship.pitt.edu/id/eprint/14157

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