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

Publication Type:
Journal Article
Citation:
Mediators of Inflammation, 2000, 9 (3-4), pp. 161 - 168
Issue Date:
2000-12-19
Full metadata record
Files in This Item:
Filename Description Size
Thumbnail2013000359OK.pdf333.34 kB
Adobe PDF
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: