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

Sukkar, MB; Margaret Hughes, J; Johnson, PRA; Armour, CL

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

Sukkar, MB

Margaret Hughes, J Johnson, PRA Armour, CL

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Publication Type:: Journal Article
Citation:: Mediators of Inflammation, 2000, 9 (3-4), pp. 161 - 168
Issue Date:: 2000-12-19

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Field	Value	Language
dc.contributor.author	Sukkar, MB https://orcid.org/0000-0003-4591-2399	en_US
dc.contributor.author	Margaret Hughes, J	en_US
dc.contributor.author	Johnson, PRA	en_US
dc.contributor.author	Armour, CL	en_US
dc.date.issued	2000-12-19	en_US
dc.identifier.citation	Mediators of Inflammation, 2000, 9 (3-4), pp. 161 - 168	en_US
dc.identifier.issn	0962-9351	en_US
dc.identifier.uri	http://hdl.handle.net/10453/74192
dc.description.abstract	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, nonallergic non-asthmatic serum (NAS) or Monomed(TM) (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 Monome(TM). IL-1β 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 Monomed(TM). 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 Monomed(TM) 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.	en_US
dc.relation.ispartof	Mediators of Inflammation	en_US
dc.subject.classification	Immunology	en_US
dc.subject.mesh	Muscle, Smooth	en_US
dc.subject.mesh	Respiratory System	en_US
dc.subject.mesh	Cells, Cultured	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Asthma	en_US
dc.subject.mesh	Tumor Necrosis Factor-alpha	en_US
dc.subject.mesh	Granulocyte-Macrophage Colony-Stimulating Factor	en_US
dc.subject.mesh	Inflammation Mediators	en_US
dc.subject.mesh	Interleukin-1	en_US
dc.subject.mesh	Cytokines	en_US
dc.subject.mesh	In Vitro Techniques	en_US
dc.title	GM-CSF production from human airway smooth muscle cells is potentiated by human serum	en_US
dc.type	Journal Article
utslib.citation.volume	3-4	en_US
utslib.citation.volume	9	en_US
utslib.for	110203 Respiratory Diseases	en_US
utslib.for	1107 Immunology	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Graduate School of Health
utslib.copyright.status	closed_access
pubs.issue	3-4	en_US
pubs.publication-status	Published	en_US
pubs.volume	9	en_US

Abstract:

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, nonallergic non-asthmatic serum (NAS) or Monomed(TM) (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 Monome(TM). IL-1β 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 Monomed(TM). 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 Monomed(TM) 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.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/26818