GM-CSF production from human airway smooth muscle cells is potentiated by human serum

Recent evidence suggests that airway smooth muscle cells (ASMC) actively participate in the airway inflammatory process in asthma. Interleukin–1β (IL–1β) and tumour necrosis factor–α (TNF–α) induce ASMC to release inflammatory mediators in vitro. ASMC mediator release in vivo, however, may be influ...

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Main Authors: Maria B. Sukkar, J. Margaret Hughes, Peter R. A. Johnson, Carol L. Armour
Format: Article
Language:English
Published: Wiley 2000-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1080/09629350020008673
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author Maria B. Sukkar
J. Margaret Hughes
Peter R. A. Johnson
Carol L. Armour
author_facet Maria B. Sukkar
J. Margaret Hughes
Peter R. A. Johnson
Carol L. Armour
author_sort Maria B. Sukkar
collection DOAJ
description Recent evidence suggests that airway smooth muscle cells (ASMC) actively participate in the airway inflammatory process in asthma. Interleukin–1β (IL–1β) and tumour necrosis factor–α (TNF–α) induce ASMC to release inflammatory mediators in vitro. ASMC mediator release in vivo, however, may be influenced by features of the allergic asthmatic phenotype. We determined whether; (1) allergic asthmatic serum (AAS) modulates ASMC mediator release in response to IL–1β and TNF–α, and (2) IL–1β/TNF–α prime ASMC to release mediators in response to AAS. IL–5 and GMCSF were quantified by ELISA in culture supernatants of; (1) ASMC pre-incubated with either AAS, non-allergic non-asthmatic serum (NAS) or MonomedTM (a serum substitute) and subsequently stimulated with IL–1β and TNF–α and (2) ASMC stimulated with IL–1β/TNF–α and subsequently exposed to either AAS, NAS or MonomedTM. IL-1g and TNF–α induced GM-CSF release in ASMC pre-incubated with AAS was not greater than that in ASMC pre-incubated with NAS or MonomedTM. IL–1β and TNF–α, however, primed ASMC to release GM-CSF in response to human serum. GM-CSF production following IL–1β/TNF–α and serum exposure (AAS or NAS) was significantly greater than that following IL–1β /TNF–α and MonomedTM exposure or IL–1β/TNF–α exposure only. Whilst the potentiating effects of human serum were not specific to allergic asthma, these findings suggest that the secretory capacity of ASMC may be up-regulated during exacerbations of asthma, where there is evidence of vascular leakage.
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spelling doaj-art-0f009fd66c2848ffb952be96a8de4c2b2025-08-20T02:02:38ZengWileyMediators of Inflammation0962-93511466-18612000-01-0193-416116810.1080/09629350020008673GM-CSF production from human airway smooth muscle cells is potentiated by human serumMaria B. Sukkar0J. Margaret Hughes1Peter R. A. Johnson2Carol L. Armour3Respiratory Research Group, Department of Pharmacy, University of Sydney, NSW 2006, AustraliaRespiratory Research Group, Department of Pharmacy, University of Sydney, NSW 2006, AustraliaRespiratory Research Group, Department of Pharmacology, University of Sydney, NSW 2006, AustraliaRespiratory Research Group, Department of Pharmacy, University of Sydney, NSW 2006, AustraliaRecent evidence suggests that airway smooth muscle cells (ASMC) actively participate in the airway inflammatory process in asthma. Interleukin–1β (IL–1β) and tumour necrosis factor–α (TNF–α) induce ASMC to release inflammatory mediators in vitro. ASMC mediator release in vivo, however, may be influenced by features of the allergic asthmatic phenotype. We determined whether; (1) allergic asthmatic serum (AAS) modulates ASMC mediator release in response to IL–1β and TNF–α, and (2) IL–1β/TNF–α prime ASMC to release mediators in response to AAS. IL–5 and GMCSF were quantified by ELISA in culture supernatants of; (1) ASMC pre-incubated with either AAS, non-allergic non-asthmatic serum (NAS) or MonomedTM (a serum substitute) and subsequently stimulated with IL–1β and TNF–α and (2) ASMC stimulated with IL–1β/TNF–α and subsequently exposed to either AAS, NAS or MonomedTM. IL-1g and TNF–α induced GM-CSF release in ASMC pre-incubated with AAS was not greater than that in ASMC pre-incubated with NAS or MonomedTM. IL–1β and TNF–α, however, primed ASMC to release GM-CSF in response to human serum. GM-CSF production following IL–1β/TNF–α and serum exposure (AAS or NAS) was significantly greater than that following IL–1β /TNF–α and MonomedTM exposure or IL–1β/TNF–α exposure only. Whilst the potentiating effects of human serum were not specific to allergic asthma, these findings suggest that the secretory capacity of ASMC may be up-regulated during exacerbations of asthma, where there is evidence of vascular leakage.http://dx.doi.org/10.1080/09629350020008673
spellingShingle Maria B. Sukkar
J. Margaret Hughes
Peter R. A. Johnson
Carol L. Armour
GM-CSF production from human airway smooth muscle cells is potentiated by human serum
Mediators of Inflammation
title GM-CSF production from human airway smooth muscle cells is potentiated by human serum
title_full GM-CSF production from human airway smooth muscle cells is potentiated by human serum
title_fullStr GM-CSF production from human airway smooth muscle cells is potentiated by human serum
title_full_unstemmed GM-CSF production from human airway smooth muscle cells is potentiated by human serum
title_short GM-CSF production from human airway smooth muscle cells is potentiated by human serum
title_sort gm csf production from human airway smooth muscle cells is potentiated by human serum
url http://dx.doi.org/10.1080/09629350020008673
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