Håkansson L, Björnsson E, Janson C, Schmekel B
Department of Clinical Chemistry, University Hospital, Uppsala, Sweden.
J Allergy Clin Immunol. 1995 Dec;96(6 Pt 1):941-50. doi: 10.1016/s0091-6749(95)70232-6.
Adhesion of peripheral blood eosinophil and neutrophil granulocytes to the endothelial cell adherence receptors E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 has been measured. The study included patients with allergic rhinitis, patients with mild allergic and nonallergic asthma, and healthy individuals; 10 persons were in each group. In addition, assay of eosinophil and neutrophil cell surface expression of the receptor complex CD11b/CD18 was performed. Increased eosinophil adhesion to vascular cell adhesion molecule-1 (p < 0.05) and intercellular adhesion molecule-1 (p < 0.05) was demonstrated in the patients with a more labile asthma, that is, a peak expiratory flow rate variability of more than 10%, suggesting a relationship to the degree of ongoing inflammation in the airways of the patients. The increased eosinophil adhesion was most probably due to a functional upregulation of the CD11b/CD18 and very late activation antigen-4 receptors, because the number of receptors measured as cell surface expression was unaltered. The increased eosinophil adhesion in the patients with high peak expiratory flow rate variability appeared independent of atopy. The increased adhesion was not entirely specific to the eosinophils, because neutrophils from patients with a peak expiratory flow rate variability of more than 10% also demonstrated increased adhesion to intercellular adhesion molecule-1 (p < 0.05) when compared with neutrophils from the patients with low peak expiratory flow rate variability. In conclusion, the demonstrated priming of eosinophil adhesion to vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 might be one contributing mechanism behind the selective accumulation of eosinophils in the lung tissue of patients with asthma.
已检测外周血嗜酸性粒细胞和中性粒细胞与内皮细胞黏附受体E-选择素、血管细胞黏附分子-1和细胞间黏附分子-1的黏附情况。该研究纳入了变应性鼻炎患者、轻度变应性和非变应性哮喘患者以及健康个体；每组10人。此外，还对受体复合物CD11b/CD18的嗜酸性粒细胞和中性粒细胞细胞表面表达进行了检测。结果显示，在哮喘病情更不稳定（即呼气峰值流速变异性超过10%）的患者中，嗜酸性粒细胞与血管细胞黏附分子-1（p<0.05）和细胞间黏附分子-1（p<0.05）的黏附增加，提示这与患者气道内炎症程度有关。嗜酸性粒细胞黏附增加很可能是由于CD11b/CD18和极晚期活化抗原-4受体的功能上调，因为以细胞表面表达衡量的受体数量未改变。呼气峰值流速变异性高的患者中嗜酸性粒细胞黏附增加似乎与特应性无关。这种黏附增加并非嗜酸性粒细胞所特有，因为与呼气峰值流速变异性低的患者的中性粒细胞相比，呼气峰值流速变异性超过10%的患者的中性粒细胞与细胞间黏附分子-1的黏附也增加（p<0.05）。总之，所证实的嗜酸性粒细胞对血管细胞黏附分子-1和细胞间黏附分子-1黏附的启动可能是哮喘患者肺组织中嗜酸性粒细胞选择性积聚背后的一种促成机制。
