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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| Format: | Article |
| Language: | English |
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Wiley
2000-01-01
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| 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. |
| format | Article |
| id | doaj-art-0f009fd66c2848ffb952be96a8de4c2b |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2000-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| 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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