Cigarette Smoke Suppresses the Surface Expression of c-kit and FcεRI on Mast Cells

Chronic obstructive pulmonary disease (COPD) is a multicomponent disease characterized by emphysema and/or chronic bronchitis. COPD is mostly associated with cigarette smoking. Cigarette smoke contains over 4,700 chemical compounds, including free radicals and LPS (a Toll-Like Receptor 4 agonist) at...

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Main Authors: M. E. Givi, B. R. Blokhuis, C. A. Da Silva, I. Adcock, J. Garssen, G. Folkerts, F. A. Redegeld, E. Mortaz
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2013/813091
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author M. E. Givi
B. R. Blokhuis
C. A. Da Silva
I. Adcock
J. Garssen
G. Folkerts
F. A. Redegeld
E. Mortaz
author_facet M. E. Givi
B. R. Blokhuis
C. A. Da Silva
I. Adcock
J. Garssen
G. Folkerts
F. A. Redegeld
E. Mortaz
author_sort M. E. Givi
collection DOAJ
description Chronic obstructive pulmonary disease (COPD) is a multicomponent disease characterized by emphysema and/or chronic bronchitis. COPD is mostly associated with cigarette smoking. Cigarette smoke contains over 4,700 chemical compounds, including free radicals and LPS (a Toll-Like Receptor 4 agonist) at concentrations which may contribute to the pathogenesis of diseases like COPD. We have previously shown that short-term exposure to cigarette smoke medium (CSM) can stimulate several inflammatory cells via TLR4 and that CSM reduces the degranulation of bone-marrow-derived mast cells (BMMCs). In the current study, the effect of CSM on mast cells maturation and function was investigated. Coculturing of BMMC with CSM during the development of bone marrow progenitor cells suppressed the granularity and the surface expression of c-kit and FcεRI receptors. Stimulation with IgE/antigen resulted in decreased degranulation and release of Th1 and Th2 cytokines. The effects of CSM exposure could not be mimicked by the addition of LPS to the culture medium. In conclusion, this study shows that CSM may affect mast cell development and subsequent response to allergic activation in a TLR4-independent manner.
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publishDate 2013-01-01
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series Mediators of Inflammation
spelling doaj-art-d977670baaa2473986a3f1fbdd6308562025-02-03T00:59:30ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/813091813091Cigarette Smoke Suppresses the Surface Expression of c-kit and FcεRI on Mast CellsM. E. Givi0B. R. Blokhuis1C. A. Da Silva2I. Adcock3J. Garssen4G. Folkerts5F. A. Redegeld6E. Mortaz7Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, 3584 CG Utrecht, The NetherlandsDivision of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, 3584 CG Utrecht, The NetherlandsIntegrative Pharmacology, Department of Biosciences, AstraZeneca R&D Lund Respiratory and Inflammation Research Area, 22 187 Lund, 43183 Mölndal, SwedenAirways Disease Section, National Heart and Lung Institute, Imperial College London, South Kensington Campus, London SW7 2AZ, UKDivision of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, 3584 CG Utrecht, The NetherlandsDivision of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, 3584 CG Utrecht, The NetherlandsDivision of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, 3584 CG Utrecht, The NetherlandsDivision of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, 3584 CG Utrecht, The NetherlandsChronic obstructive pulmonary disease (COPD) is a multicomponent disease characterized by emphysema and/or chronic bronchitis. COPD is mostly associated with cigarette smoking. Cigarette smoke contains over 4,700 chemical compounds, including free radicals and LPS (a Toll-Like Receptor 4 agonist) at concentrations which may contribute to the pathogenesis of diseases like COPD. We have previously shown that short-term exposure to cigarette smoke medium (CSM) can stimulate several inflammatory cells via TLR4 and that CSM reduces the degranulation of bone-marrow-derived mast cells (BMMCs). In the current study, the effect of CSM on mast cells maturation and function was investigated. Coculturing of BMMC with CSM during the development of bone marrow progenitor cells suppressed the granularity and the surface expression of c-kit and FcεRI receptors. Stimulation with IgE/antigen resulted in decreased degranulation and release of Th1 and Th2 cytokines. The effects of CSM exposure could not be mimicked by the addition of LPS to the culture medium. In conclusion, this study shows that CSM may affect mast cell development and subsequent response to allergic activation in a TLR4-independent manner.http://dx.doi.org/10.1155/2013/813091
spellingShingle M. E. Givi
B. R. Blokhuis
C. A. Da Silva
I. Adcock
J. Garssen
G. Folkerts
F. A. Redegeld
E. Mortaz
Cigarette Smoke Suppresses the Surface Expression of c-kit and FcεRI on Mast Cells
Mediators of Inflammation
title Cigarette Smoke Suppresses the Surface Expression of c-kit and FcεRI on Mast Cells
title_full Cigarette Smoke Suppresses the Surface Expression of c-kit and FcεRI on Mast Cells
title_fullStr Cigarette Smoke Suppresses the Surface Expression of c-kit and FcεRI on Mast Cells
title_full_unstemmed Cigarette Smoke Suppresses the Surface Expression of c-kit and FcεRI on Mast Cells
title_short Cigarette Smoke Suppresses the Surface Expression of c-kit and FcεRI on Mast Cells
title_sort cigarette smoke suppresses the surface expression of c kit and fcεri on mast cells
url http://dx.doi.org/10.1155/2013/813091
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