Enhancement of goblet cell hyperplasia and airway hyperresponsiveness by salbutamol in a rat model of atopic asthma
A Kamachia, M Munakatab, Y Nasuharaa, M Nishimuraa, Y Ohtsukab, M Amishimaa, T Takahashia, Y Hommac, Y Kawakamia
a First Department of
Medicine, School of Medicine, Hokkaido University, Sapporo, Japan, b The Department of Pulmonary Medicine, School of
Medicine, Fukushima Medical University, Fukushima, Japan, c The Medical
Administration Center, School of Medicine, Hokkaido University
Correspondence to: Dr A Kamachi, First Department of Medicine, School of Medicine, Hokkaido University N-15, W-7 Kita-ku, Sapporo, 060-8638 Japan caw35770{at}pop21.odn.ne.jp
Received 3 March 2000; Returned to authors 19 July 2000; Revised version received 25 August 2000; Accepted for publication 25 September 2000
BACKGROUND
Goblet cell
hyperplasia (GCH) is a prominent feature in animal models of atopic
asthma produced by immunisation and following multiple challenges with
antigens. The aim of this study was to examine the effect of a
2 agonist on the development of GCH induced by the
immune response.
METHODSBrown Norway
rats were immunised and challenged with an aerosol of ovalbumin for
four weeks. Salbutamol (0.5 mg/kg/day) or vehicle was continuously
delivered for the four weeks using a subcutaneously implanted osmotic
minipump. The density of goblet cells, other morphological changes,
and airway responsiveness to methacholine were evaluated 24 hours after
the final challenge.
RESULTSTreatment with
salbutamol induced a more than twofold increase in the mean (SE) number
of goblet cells (53.7 (7.3) vs 114.5 (11.8) cells/103
epithelial cells, p<0.01) while it did not significantly influence airway wall thickening and eosinophilic infiltration. Airway
responsiveness to methacholine expressed as the logarithmic value of
the concentration of methacholine required to generate a 50% increase
in airway pressure (logPC150Mch) was also enhanced by the
2 agonist (-0.56 (0.21) vs -0.95 (0.05), p<0.05).
Additional experiments revealed that the same dose of the
2 agonist alone did not cause GCH in non-immunised rats
and that the enhancement of GCH by salbutamol was completely abolished
by simultaneous treatment with methylprednisolone (0.5 mg/kg/day).
CONCLUSIONSThese data
suggest that salbutamol enhances goblet cell hyperplasia and airway
hyperresponsiveness in this rat model of atopic asthma.
Keywords: bronchial asthma; salbutamol; goblet cell hyperplasia
© 2001 by Thorax
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