Document Detail


Vasoactive intestinal peptide (VIP) receptor expression in monocyte-derived macrophages from COPD patients.
MedLine Citation:
PMID:  20026142     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Vasoactive intestinal peptide (VIP) is one of the most abundant molecules found in the respiratory tract. Due to its anti-inflammatory and bronchodilatatory properties, it has been proposed as a novel treatment for chronic obstructive pulmonary disease (COPD). The actions of VIP are mediated via three different G-protein-coupled receptors (VPAC1, VPAC2 and PAC1) which are expressed in the respiratory tract and on immunocompetent cells including macrophages. Alveolar macrophages (AM) are key players in the pathogenesis of COPD and contribute to the severity and progression of the disease. While VPAC1 has been reported to be elevated in subepithelial cells in smokers with chronic bronchitis, little is known about VPAC expression of AM in COPD patients. AM from COPD patients show a strong VPAC1 expression which exceeds VPAC2. A similar receptor expression pattern was also observed in lipopolysaccharide (LPS)-activated monocyte-derived macrophages (MDM) from healthy volunteers and COPD patients. VIP has been shown to down-regulate interleukin 8 (IL-8) secretion significantly in MDM after LPS stimulation. The response to VIP was similar in MDM from COPD patients and healthy volunteers. Our results indicate that VPAC1 up-regulation in macrophages is a common mechanism in response to acute and chronic pro-inflammatory stimuli. Although VPAC1 up-regulation is dominant, both receptor subtypes are necessary for optimal anti-inflammatory signaling. The high VPAC1 expression in AM may reflect the chronic pro-inflammatory environment found in the lung of COPD patients. Treatment with VIP may help to decrease the chronic inflammation in the lung of COPD patients.
Authors:
Bernhard Burian; Angela Storka; Beatrice A Marzluf; Yong-Cheng Yen; Christopher Lambers; Bruno Robibaro; Karin Vonbank; Wilhelm Mosgoeller; Ventzislav Petkov
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-12-22
Journal Detail:
Title:  Peptides     Volume:  31     ISSN:  1873-5169     ISO Abbreviation:  Peptides     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-03-12     Completed Date:  2010-07-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8008690     Medline TA:  Peptides     Country:  United States    
Other Details:
Languages:  eng     Pagination:  603-8     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2009 Elsevier Inc. All rights reserved.
Affiliation:
Medical University of Vienna, Department of Internal Medicine II, Division of Pulmonary Medicine, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
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MeSH Terms
Descriptor/Qualifier:
Aged
Animals
Female
Humans
Inflammation / immunology
Interleukin-8 / immunology
Lipopolysaccharides / immunology,  pharmacology
Lung / cytology,  immunology
Macrophages / cytology,  drug effects,  immunology*
Male
Middle Aged
Pulmonary Disease, Chronic Obstructive / immunology*
Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I / genetics,  immunology*
Receptors, Vasoactive Intestinal Peptide, Type II / genetics,  immunology*
Receptors, Vasoactive Intestinal Polypeptide, Type I / genetics,  immunology*
Signal Transduction / immunology
Chemical
Reg. No./Substance:
0/Interleukin-8; 0/Lipopolysaccharides; 0/Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I; 0/Receptors, Vasoactive Intestinal Peptide, Type II; 0/Receptors, Vasoactive Intestinal Polypeptide, Type I

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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