| IntroductionAt present , glucocorticoids are potent anti - inflammatory drugs in the asthma therapy but not well known to treat mechanisms. Eflfects of glucocorticoids to inflammatory cells apoptosis was the focus of asthma. Now, many studies are limited inflammatory cells apoptosis in blood of asthma, rarely in sputum . Because inhaled glucocorticoid acts airway directly, the measures of inflammation effctor cells apoptosis in the air inflammation of bronchial asthma is thought to be critically relevent in treat mechanisms of glucocorticoids. To investigate the effects of glucocorticoid on the rate of apoptosis in eosinophils and neutrophils by induced sputum of topic asthmatic patients ,We do this test to compare with the results before and after treatment with glucocorticoid.Subjects and methods20 mild to moderate asthmatic subjects were recruited from our hospital between November in 2002 and April in 2003. The patients with asthma all had symptoms of episodic chest tightness, wheezing and dyspnea; the diagnosis of asthma was supported by standard of asthma in China in 1997. Eleven patients are male, nine are female, mean age 41 11 years, who had not previously received glucocorticoid treatment. They were induced sputum before glucocorticoid treatment and measured respiratory function and the rate of apoptosis in eosinophils and neutrophils, respectively. They were A group. After inhaled glucocorticoid treatment for 4 weeks , respiratory function and the rate of apoptosis in eosinophils and neutrophils were measured by flow cytometry, respectively . They were B group.The methods of sputum collected and treated were carried out by Hansel TT and colleagues. The measure of cells apoptosis follows introduction of the apoptosis kit. The results of respiratory function are by respiratory function machine. Induced sputum is an aerosol of hypertonic saline.Apoptosis results: Cells that are in early eosinophil apoptosis are CD9PerCP - Cy 5.5 positive, Annexin V - FITC positive,and PI negative. Cells that are in early neutrophil apoptosis are CD9PerCP - Cy negative 5.5, Annexin V - FITC positive and PI negative.Apoptosis rate is expressed as apoptotic index (number of apoptotic cells/ total number of cells).Statistical analysis:Paired t -tests was used to campare by SPSS 11.0.ResultsGlucocorticoid treatment was associated with an increase in the mean FEV1, FVC,%FEV1 ,FEV/FVC,V50(P <0.05) , but V2 no change.The number of eosinophil was 1850 928before and 874 191 after glu-cocorticoid treatment. The rate of eosinophil apoptosis was ( 10. 24 7. 53)% before and (25. 03 13. 98) % after glucocorticoid treatment. However, the number of neutrophil was 2481 1307,2733 1049 and neutrophil apoptosis was ( 16. 40 11. 88 ) % , ( 15. 25 10. 05 ) % before and after treatment , respectively. After glucocorticoid treatment, the mean number eosinophil decreased significantly; the rate of apoptosis eosinophil increased significantly, but no significant change in the number of neutrophil and apoptosis neutrophils were oberved.DissussionInhaled glucocorticoid decreased significantly the mean percentage of eosinophil in sputum samples and increased the rate of apoptosis of eosinophils . The results are same as others in blood. So whatever in blood or in sputum, glucocorticoid increased the rate of apoptosis of eosinophil. In present study, glu-cocorticoid induce eosinophil apoptosis via an effect on glucocorticoid receptor. A potent evidence is that an antagonist of glucocorticoid receptor mifepristone can reverse the apoptosis promoting effects of glucocorticoid on eosinophil. Other studies found glucocorticoid - resistant asthmatic subjects might exist the decrease of down - regulate receptor. The induction of eosinophil apoptosis may be one of the anti - inflammatory mechanisms of glucocorticoids in asthma or allergy. We also found glucocorticoids can increase respiratory function in big airway, but improvement of small airway no change. It suggest the function of small airway increasing n... |
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