THE MECHANISMS OF AIRWAY REMODELING IN BRONCHIAL ASTHMA.

“阿斯卡利斯-一个有标记的累积，特别是有标记的累积。”“伊osinophil渗透到了次要的mucosa和goblet细胞hyperplasia从中央机场扩散到较小机场，以及在较小机场中被标记的变化。”这些变化是一致的，因为这些变化是在病人身上观察到的，是用哮喘开发出来的，以便对机场进行改装。However，基础薄膜的明显反应，空气中光滑的肌肉超囊症，以及在这个动物模型中观察到的亚多尺度地面上不观察到的asthmatic airway remodeling没有观察到。要建立一个asthmatic airway remodeling的动物模型，更进一步的测试可能是必要的。在临床研究中，我们在患者体内测量了炎症细胞、ECP、tryptase和TGF-beta，以及受诱导的天然气和挥发的硝酸氧化物（ENO）中的TGF-β ... More 我的哮喘，并通过航空重塑来测试我们的关系。航空路改装的存在得到了固定的气流限制和支气管壁厚度（rt.B1）的评估，并使用Chest HRCT。在asthmatics，eosinophil编号和ECP的水平，TGF-beta比那些在健康对象中的更重要。一些哮喘在人造卫星中展示了更高的tryptase水平。不管怎样，在这些炎症细胞和介质之间，在有和没有有气道重新建模的哮喘之间没有明显的区别，而且在人造卫星中，TGF-beta有一个趋势，以增加与重新建模的哮喘。ENO对空气压力的增加的依赖性和生产在空气压力中明显高于那些在健康物体中的哮喘。ENO in asthmatics was significantly correlated positively with eosinophilia in sputum and negatively with FEVイイD21イエD2.“ENO在与航空路重构的asthmatics中的集中和生产明显低于没有航空路重构的那些，在两个群体之间的人造碘化症中没有明显的区别。”这已经被认为是一个可持续的生态学航空通货膨胀可能与航空器改装的发展有关的问题。“Eosinophilic炎症评估的诱导性假脱机和假脱机酶和TGF-beta的水平可能是不可能预测航空路重构的存在，如何，对卫星Eosinophilia和ENO生产的不确定性可能预测航空路重构的存在。”Less（低）

The inhalation of Ascaris suum twice a week for 8 weeks induced a marked accumulation in the airway of inflammatory cells, especially eosinophils, and goblet cell hyperplasia of epithelial cell in allergic sheep naturally sensitized by Ascaris. The eosinophil infiltration into the subepithelial mucosa and goblet cell hyperplasia were distributed from central airway to the small airway, and the changes were marked in the small airways. These changes are consistent with the changes observed in the patient with asthma developed to the airway remodeling. However, the apparent thickening of basement membrane, airway smooth muscle hyperplasia, and increase in submucosal glands observed in asthmatic airway remodeling were not observed in this animal model. To establish animal model of asthmatic airway remodeling, further examination may be needed. In clinical study, we measured the inflammatory cells, ECP, tryptase, and TGF-beta in induced sputum and exhaled nitric oxide (ENO) in patients wit … More h asthma, and examined the relationship with airway remodeling. The presence of airway remodeling was assessed by fixed airflow limitation and bronchial wall thickness (rt. B1) evaluated by using a chest HRCT. In asthmatics, the eosinophil numbers and the levels of ECP, TGF-beta were significantly higher than those in healthy subjects. Some asthmatics showed a higher tryptase level in sputum. However, there was no significant difference in these inflammatory cells and mediators between the asthmatics with and without airway remodeling, however, the level of TGF-beta in sputum had a tendency to increase in asthmatics with remodeling. The concentration and production of ENO dependent on the increase in airway pressure were significantly higher in asthmatics than those in healthy subjects. The ENO in asthmatics was significantly correlated positively with eosinophilia in sputum and negatively with FEVィイD21ィエD2. The concentration and production of ENO in asthmatics with airway remodeling were significantly lower than those in asthmatics without airway remodeling, whereas there was no significant difference in sputum eosinophilia between the two groups. It has been suggested that a sustaining eosinophilic airway inflammation may be associated with the development of airway remodeling. The eosinophilic inflammation evaluated induced sputum and the level of tryptase and TGF-beta in sputum may not be able to predict the presence of airway remodeling, however, the discrepancy of sputum eosinophilia and ENO production may be predicted the presence of airway remodeling. Less