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-induced eotaxin release from cultured human airway smooth muscle cells by ß2-agonists and corticosteroids
Division of Respiratory Medicine, City Hospital, University of Nottingham, Nottingham, U.K.
1Correspondence: Division of Respiratory Medicine, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham NG5 1PB, U.K. E-mail: mfzlp{at}unix.ccc.nottingham.ac.uk or alan.knox{at}nottingham.ac.uk
Eotaxin is a potent eosinophil chemoattractant that contributes to the
eosinophilia seen in asthma and other allergic disorders. Recent
studies have identified human airway smooth muscle (HASM) as a rich
source of eotaxin, but the factors regulating its production are poorly
understood. Here we describe for the first time that
ß2-agonists can inhibit cytokine-induced eotaxin release.
We found that TNF-
stimulated eotaxin release (assayed by ELISA)
from HASM cells and that the release was partially inhibited by
salbutamol and salmeterol. The effect of ß2-agonists was
mimicked by forskolin and 8-bromo-cAMP and potentiated by the
cAMP-dependent phosphodiesterase inhibitor rolipram, suggesting that it
is cAMP dependent. We also found that the cAMP inhibition was likely at
the transcription stage, although experiments with the PKA inhibitors
H-89 and Rp-cAMP or the PKG inhibitor KT5823 suggested that none of
these kinases was involved. Partial inhibition of eotaxin release was
also seen with the corticosteroids dexamethasone and fluticasone. The
combined use of ß2-agonists, rolipram, and steroids
abolished TNF--induced eotaxin release. These results suggest that
the combination of a ß2-agonist, PDE inhibitor, and a
corticosteroid may have additive beneficial effects in the treatment of
the eosinophilia associated with asthma and other allergic
diseases—Pang, L., Knox, A. J. Regulation of TNF--induced
eotaxin release from cultured human airway smooth muscle cells by
ß2-agonists and corticosteroids.
Key Words: eosinophil • cyclic AMP • asthma • phosphodiesterase • cytokine
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