MORPHOLOGICAL CHANGES OF AIRWAY REMODELING AND AIRWAY INFLAMMATION IN BRONCHIAL ASTHMA

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The aim of this study was to evaluate airway wall thickness and air trapping by means of High-Resolution Computed Tomography ( HRCT ) in asymptomatic asthmatics showing fixed airflow obstruction. The bronchial wall thickness of the right B1 bronchus and air trapping which were assessed in terms of the ratio of CT numbers in the lung fields at full expiration and inspiration ( E/I ratio ), were evaluated by means of HRCT of 24 stable and asymptomatic asthmatics. Prior to the HRCT examination, all patients were treated with inhaled corticosteroids /and oral corticosteroids for at least 6 months, and then were given 20mcg procaterol hydrocloride to inhale 15min before CT scanning. In 14 patients who showed fixed airflow obstruction ( % FEV_1 <80 % or/and FEV_<1%> <70 % ) 15 min after the inhalation of β_2 agonists, the wall thickness and % wall area of vertical section of rt. B1 and E/I ratio were significantly greater than those in 10 patients who showed normal spirometric results after … More the inhalation. The wall thickness, % wall area, and E/I ratios showed significantly negative correlation with % FEV_1 measured 15 min after the inhalation ofa bronchodilator. The E/I ratio was also showed significantly positive correlation with the wall thickness and % wall area. These findings suggest that irreversible structural changes of the airway wall may occur not only in large but also in small airways in asthmatics with fixed airflow obstruction. This means that evaluation of airway wall thickness at rt. B I bronchus and air trapping by HRCT in asthmatics may provide a useful and non-invasive means of assessing structural changes in airways.Ca^<2+> activated chloride channel ( CLCA ) family, which is considered to be associated with airway hyperreactivity and mucous overproduction, has been demonstrated to express in airway epithelia in sensitized mouse. In order to examine whether the CLCA1, one of the CLCA families, participates as one factor contributing to mucous overproduction or airway hyperreactivity in patients with bronchial asthma, we measured mRNA expression of CLCA1 on the induced-sputum cells obtained from 21 patients with asthma and 13 healthy non-smokers. Sputum was induced by the inhalation of hypertonic saline. The obtained sputum was incubated with 0.1 mM DTT, and sputum cells were purified. The purified sputum cells were mixed with ISOGEN.RNA from sputum cells was extracted and purified, and lOOng RNA was reverse transcribed using TaqMan Gold RT-PCR Kit. _CDNA samples corresponding 10 ng of total RNA were measured by real-time quantitative PCR using a sequence detection instrument. The copies of CLCA1 gene corrected by the copies of GAPDH gene were calculated. The expressions of CLCA1 corrected by GAPDH of sputum cells from asthma and healthy non-smokers were 256.2±89.2 and 73.3±25.6 ( CLCA1X 10^4 copies/GAPDH copies ). The expression of CLCA1 gene had a tendency to be higher compared with those in healthy non-smokers, but there was no significant difference. There were no significant associations between the CLCA1 gene expression and severity, ill length, pulmonary functions, and sputum eosinophilia. These findings suggest that CLCA1 gene may be not so importantly contribute to the pathogenesis of asthma, and further examination was needed. Less