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Thorax 2001;56:19-24 doi:10.1136/thorax.56.1.19
  • Original article

Enhancement of goblet cell hyperplasia and airway hyperresponsiveness by salbutamol in a rat model of atopic asthma

  1. A Kamachia,
  2. M Munakatab,
  3. Y Nasuharaa,
  4. M Nishimuraa,
  5. Y Ohtsukab,
  6. M Amishimaa,
  7. T Takahashia,
  8. Y Hommac,
  9. Y Kawakamia
  1. aFirst Department of Medicine, School of Medicine, Hokkaido University, Sapporo, Japan, bThe Department of Pulmonary Medicine, School of Medicine, Fukushima Medical University, Fukushima, Japan, cThe Medical Administration Center, School of Medicine, Hokkaido University
  1. Dr A Kamachi, First Department of Medicine, School of Medicine, Hokkaido University N-15, W-7 Kita-ku, Sapporo, 060-8638 Japancaw35770{at}pop21.odn.ne.jp
  • Received 3 March 2000
  • Revision requested 19 July 2000
  • Revised 25 August 2000
  • Accepted 25 September 2000

Abstract

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 β2 agonist on the development of GCH induced by the immune response.

METHODS Brown 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.

RESULTS Treatment 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/103epithelial 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 β2 agonist (–0.56 (0.21) vs –0.95 (0.05), p<0.05). Additional experiments revealed that the same dose of the β2 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).

CONCLUSIONS These data suggest that salbutamol enhances goblet cell hyperplasia and airway hyperresponsiveness in this rat model of atopic asthma.

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