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- Title
GM-CSF production from human airway smooth muscle cells is potentiated by human serum.
- Authors
Sukkar, Maria B.; Hughes, J. Margaret; Johnson, Peter R. A.; Armour, Carol L.
- 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, non-allergic non-asthmatic serum (NAS) or Monomed™(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 Monomed™. 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™. 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-1 beta /TNF- alpha and Monomed™ 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.
- Subjects
PHENOTYPES; ASTHMA; SMOOTH muscle
- Publication
Mediators of Inflammation, 2000, Vol 9, Issue 3/4, p161
- ISSN
0962-9351
- Publication type
Article
- DOI
10.1080/09629350020008673