PT  - JOURNAL ARTICLE
AU  - A Kamachi
AU  - M Munakata
AU  - Y Nasuhara
AU  - M Nishimura
AU  - Y Ohtsuka
AU  - M Amishima
AU  - T Takahashi
AU  - Y Homma
AU  - Y Kawakami
TI  - Enhancement of goblet cell hyperplasia and airway hyperresponsiveness by salbutamol in a rat model of atopic asthma
AID  - 10.1136/thorax.56.1.19
DP  - 2001 Jan 01
TA  - Thorax
PG  - 19--24
VI  - 56
IP  - 1
4099  - http://thorax.bmj.com/content/56/1/19.short
4100  - http://thorax.bmj.com/content/56/1/19.full
SO  - Thorax2001 Jan 01; 56
AB  - 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.