哮喘气道炎症粘附机制的实验研究

Experimental study on adhesion mechanism of airway inflammation in the pathogenesis of bronchial asthma

目的评价细胞间粘附分子１（ＩＣＡＭ１）、Ｐ选择素在哮喘气道炎症粘附机制中的作用，进一步阐明哮喘的发病机理。方法用酶联免疫吸附试验、肺组织免疫组化检查和呼吸生理学方法系统观察正常组和哮喘组豚鼠各项指标。结果（１）哮喘组豚鼠肺潮气量、动态肺顺应性（Ｃｄｙｎ）和肺气道阻力与对照组比较差异有显著性（Ｐ＜０．０１及Ｐ＜０．０５）。（２）哮喘组豚鼠血浆和肺泡灌洗液（ＢＡＬＦ）可溶性ＩＣＡＭ１（ｓＩＣＡＭ１）、可溶性Ｐ选择素、血清和ＢＡＬＦ嗜酸粒细胞阳离子蛋白（ＥＣＰ）与对照组比较，差异有显著性（Ｐ＜０．０１）；ＢＡＬＦ中白细胞介素８（ＩＬ８）与对照组比较差异也有显著性（Ｐ＜０．０１）。（３）哮喘组豚鼠肺组织（气道上皮和血管内皮）ＩＣＡＭ１和ＩＬ８表达与对照组比较，差异有显著性（Ｐ＜０．０１）。结论ＩＣＡＭ１、Ｐ选择素、ＩＬ８。

Objective To investigate the adhesive mechanism of airway inflammation in the pathogenesis of asthma. Methods The guniea pigs were divided into 2 groups,the asthmatic animal group and the normal animal group.The following tests were performed: (a) The values of sICAM 1,sP selectin,IL 8 and ECP both in plasma (or serum) and BALF were measured by ELISA.(b) The expressions of ICAM 1 and IL 8 on the bronchial epithelial cells and vascular endothelial cells were measured by immuno histochemistry staining.(c) The lung functions(VT,Cdyn,R L)were tested. Results (a) The values of sICAM 1,sP selectin and ECP were elevated both in the plasma and BALF level of asthmatic group ( P <0.01). Additionally,IL 8 of BALF level of asthmatic group was elevated ( P <0.01), while IL 8 of serum level was lower than that of normal group( P <0.01). (b)The expressions of ICAM 1,IL 8 on the bronchial epithelial and vascular endothelial cells in asthmatic animals were up regulated ( P <0.01). (c) The lung functions of the asthmatic animals were impaired (V T,C dyn P <0.01;R L P <0.05). Conclusions ALL the results above suggests that ICAM 1,IL 8,P selectin and ECP are involved in the inflammative adhesive mechanism of asthma.