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Inflammatory Pharmacology, AstraZeneca, Lund, Sweden
CORRESPONDENCE: R. Bratts and AstraZeneca R&D Operations, S-22187, Lund, Sweden. Fax: 46 46336624
Keywords: budesonide, ß2-agonist and glucocorticoid interactions, formoterol, granulocyte macrophage-colony stimulating factor, interleukin-8, triggered bronchial epithelial cells
Received: August 24, 2000
Accepted March 19, 2001
The effect of formoterol, alone and in combination with budesonide, upon tumour necrosis factor-
Addition of formoterol (
In conclusion, the combination of budesonide and formoterol reduces the secretion of granulocyte macrophage-colony stimulating factor to basal levels and counteracts the capacity of formoterol alone to induce interleukin-8 production, modulations which may facilitate improved asthma control.
stimulated (10 ng·mL–1) human bronchial epithelial cells was investigated. 
10–10 M) reduced granulocyte macrophage-colony stimulating factor (GM-CSF) levels, as assessed by enzyme-linked immunosorbent assay, by 40–50% and increased interleukin (IL)-8 levels by 
50%. The effects of formoterol were long lasting (23 h). Budesonide (10–8 M) reduced the amounts of both cytokines (GM-CSF and IL-8) by 40%. Simultaneous addition of formoterol and budesonide reduced GM-CSF levels 75%, while IL-8 levels were decreased 40%, similar to the reduction obtained with budesonide alone. The glucocorticoid receptor (GR) antagonist RU486 did not influence the effect of formoterol, suggesting no involvement of the GR. Formoterol rapidly induced an elevation in intracellular cyclic adenosine monophosphate, which was reduced in the presence of propranolol. In addition, the alterations in cytokine secretion induced by formoterol could be fully blocked by propranolol, demonstrating that these effects are ß2-receptor mediated.
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