Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype
<p>Abstract</p> <p>Background</p> <p>A major feature of chronic obstructive pulmonary disease (COPD) is airway remodelling, which includes an increased airway smooth muscle (ASM) mass. The mechanisms underlying ASM remodelling in COPD are currently unknown. We hypothesi...
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Format: | Article |
Language: | English |
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BMC
2010-04-01
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Series: | Respiratory Research |
Online Access: | http://respiratory-research.com/content/11/1/48 |
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author | Zaagsma Johan Toorn Marco Sami Riham Lesterhuis Andries H Gosens Reinoud Pera Tonio Meurs Herman |
author_facet | Zaagsma Johan Toorn Marco Sami Riham Lesterhuis Andries H Gosens Reinoud Pera Tonio Meurs Herman |
author_sort | Zaagsma Johan |
collection | DOAJ |
description | <p>Abstract</p> <p>Background</p> <p>A major feature of chronic obstructive pulmonary disease (COPD) is airway remodelling, which includes an increased airway smooth muscle (ASM) mass. The mechanisms underlying ASM remodelling in COPD are currently unknown. We hypothesized that cigarette smoke (CS) and/or lipopolysaccharide (LPS), a major constituent of CS, organic dust and gram-negative bacteria, that may be involved in recurrent airway infections and exacerbations in COPD patients, would induce phenotype changes of ASM.</p> <p>Methods</p> <p>To this aim, using cultured bovine tracheal smooth muscle (BTSM) cells and tissue, we investigated the direct effects of CS extract (CSE) and LPS on ASM proliferation and contractility.</p> <p>Results</p> <p>Both CSE and LPS induced a profound and concentration-dependent increase in DNA synthesis in BTSM cells. CSE and LPS also induced a significant increase in BTSM cell number, which was associated with increased cyclin D1 expression and dependent on activation of ERK 1/2 and p38 MAP kinase. Consistent with a shift to a more proliferative phenotype, prolonged treatment of BTSM strips with CSE or LPS significantly decreased maximal methacholine- and KCl-induced contraction.</p> <p>Conclusions</p> <p>Direct exposure of ASM to CSE or LPS causes the induction of a proliferative, hypocontractile ASM phenotype, which may be involved in airway remodelling in COPD.</p> |
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institution | Directory Open Access Journal |
issn | 1465-9921 |
language | English |
last_indexed | 2024-12-13T20:44:58Z |
publishDate | 2010-04-01 |
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series | Respiratory Research |
spelling | doaj.art-b7d9ee06b5384b2086b401751ffa4fe92022-12-21T23:32:03ZengBMCRespiratory Research1465-99212010-04-011114810.1186/1465-9921-11-48Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotypeZaagsma JohanToorn MarcoSami RihamLesterhuis Andries HGosens ReinoudPera TonioMeurs Herman<p>Abstract</p> <p>Background</p> <p>A major feature of chronic obstructive pulmonary disease (COPD) is airway remodelling, which includes an increased airway smooth muscle (ASM) mass. The mechanisms underlying ASM remodelling in COPD are currently unknown. We hypothesized that cigarette smoke (CS) and/or lipopolysaccharide (LPS), a major constituent of CS, organic dust and gram-negative bacteria, that may be involved in recurrent airway infections and exacerbations in COPD patients, would induce phenotype changes of ASM.</p> <p>Methods</p> <p>To this aim, using cultured bovine tracheal smooth muscle (BTSM) cells and tissue, we investigated the direct effects of CS extract (CSE) and LPS on ASM proliferation and contractility.</p> <p>Results</p> <p>Both CSE and LPS induced a profound and concentration-dependent increase in DNA synthesis in BTSM cells. CSE and LPS also induced a significant increase in BTSM cell number, which was associated with increased cyclin D1 expression and dependent on activation of ERK 1/2 and p38 MAP kinase. Consistent with a shift to a more proliferative phenotype, prolonged treatment of BTSM strips with CSE or LPS significantly decreased maximal methacholine- and KCl-induced contraction.</p> <p>Conclusions</p> <p>Direct exposure of ASM to CSE or LPS causes the induction of a proliferative, hypocontractile ASM phenotype, which may be involved in airway remodelling in COPD.</p>http://respiratory-research.com/content/11/1/48 |
spellingShingle | Zaagsma Johan Toorn Marco Sami Riham Lesterhuis Andries H Gosens Reinoud Pera Tonio Meurs Herman Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype Respiratory Research |
title | Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype |
title_full | Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype |
title_fullStr | Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype |
title_full_unstemmed | Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype |
title_short | Cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype |
title_sort | cigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotype |
url | http://respiratory-research.com/content/11/1/48 |
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