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agonist and corticosteroid treatment on
nuclear transcription factors in bronchial mucosa in asthma
a Department of
Respiratory Medicine, Dunedin School of Medicine, University of Otago,
New Zealand, b National Heart & Lung Institute, London SW3 6LY,
UK
Correspondence to: Dr D R Taylor, Department of Medicine, Dunedin School of Medicine, PO Box 913, Dunedin, New Zealand.
Received 2 March 1998; Returned to authors 25 August 1998; Revised version received 11 February 1999; Accepted for publication 11 February 1999
BACKGROUND
Inhaled
corticosteroids and 
agonists are the most commonly used treatments
in asthma and are often used together. Recent evidence suggests that
many of the anti-inflammatory actions of corticosteroids are mediated
by cross-talk between the activated glucocorticoid receptor (GR) and
other transcription factors such as the pro-inflammatory nuclear factor
kappa B (NF
B). Beta agonists can activate the transcription factor
cAMP response element binding protein (CREB). A mutual inhibition
between GR and CREB occurs in vitro which raises the possibility of a
negative interaction between corticosteroid and agonist drugs. A
study was undertaken to determine whether these interactions occur
during treatment with 2 agonists and corticosteroids in asthma.
METHODSSeven subjects
who were participating in a randomised, placebo controlled, crossover
study of six weeks treatment with inhaled budesonide (400 µg twice
daily), terbutaline (1 mg four times daily), and combined treatment
were recruited. Biopsy samples of the bronchial mucosa were obtained
after each treatment and analysed for the DNA binding activity of GR,
CREB, and NFB.
RESULTSBudesonide
increased GR activity (p<0.05) and decreased NFB activity
(p<0.05). No treatment combination altered CREB activity and
terbutaline had no significant effects on any transcription factor.
CONCLUSIONSInhaled
corticosteroids have significant effects on GR and NFB activity in
bronchial mucosa. A negative interaction between inhaled
corticosteroids and agonists was not found.
2 agonists;
transcription factors
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