哮喘大鼠鼻内慢性给予烟曲霉芽孢导致气道重塑和炎症恶化
2009/05/13
背景和目的：流行病学证据显示，真菌暴露和哮喘的恶化之间密切相关。然而，真菌作为哮喘发生和发展的一个外源性促进物，其具体作用尚不完全清楚。本实验在大鼠慢性哮喘模型中研究烟曲霉暴露对气道重塑和炎症的影响。
方法：通过全身致敏和反复给予卵清蛋白（OVA）建立大鼠慢性哮喘模型。大鼠鼻内慢性吸入烟曲霉芽孢，检测气道炎症、气道重塑和BHR。
结果：哮喘大鼠慢性吸入烟曲霉芽孢能增加T辅助细胞2（Th2）细胞因子的产生，增加总血清IgE 浓度，导致气道嗜酸性粒细胞聚集和淋巴细胞浸润。同时，吸入烟曲霉芽孢能导致杯状细胞异常增生、粘液产生过多以及上皮下胶原沉积。哮喘大鼠吸入真菌导致的气道重塑与BHR平行。
结论：在OVA致敏的哮喘大鼠中，烟曲霉的慢性暴露能恶化Th2气道炎症，促进气道重塑和增加BHR。
（苏楠 审校）
Gao FS, et al. Respirology. 2009 Feb 4. [Epub ahead of print]
Chronic intranasal administration of Aspergillus fumigatus spores leads to aggravation of airway inflammation and remodelling in asthmatic rats.
Background and objective: Epidemiological evidence indicates a close link between exposure to fungi and deterioration of asthma. However, the role of fungi as an exogenous precipitant for initiation and progression of asthma has been incompletely explored. In this study, the effects of Aspergillus fumigatus exposure on airway inflammation and remodelling in a rat model of chronic asthma were investigated.
Methods: The rat model of chronic asthma was established by systemic sensitization and repeated challenge with ovalbumin (OVA). The asthmatic rats were exposed to chronic intranasal inhalation of A. fumigatus spores. Changes in airway inflammation, remodelling and BHR were measured after exposure to the fungus.
Results: Chronic inhalation of A. fumigatus spores elevated the production of T helper 2 (Th2) cytokines, increased the concentration of total serum IgE, and resulted in the recruitment of eosinophils and lymphocyte infiltration into the airways of asthmatic rats. Goblet cell hyperplasia, mucus hyperproduction and subepithelial collagen deposition were also induced by inhalation of the fungus. The remodelling changes induced by inhalation of the fungus paralleled the changes in BHR in this rat model of asthma.
Conclusions: Chronic exposure to A. fumigatus aggravated Th2 airway inflammation, promoted airway remodelling and increased BHR in OVA-sensitized and -challenged rats.
