Chihara J
Department of Clinical and Laboratory Medicine, Akita University School of Medicine.
Rinsho Byori. 1997 Jun;45(6):519-27.
Recently, adhesion molecules, as well as eosinophils, have been found to play an important role in the inflammatory processes in allergic disease. We demonstrated here as below. Characteristics of adhesion molecules expression on eosinophils in asthma, namely, high-intensity expression of adhesion molecules. Induction of adhesion molecule expression by PAF and RANTES and in addition induction by the supernatant of mononuclear cells from mite-allergic asthmatic patients stimulated with mite-allergen as well as with a combination of the recombinant IL-3, GM-CSF and IL-5. Elevated soluble ICAM-1 in bronchial asthma. Moreover, the presence of a large variety of membrane receptors and the identification of cytotoxic molecules (mainly granule basic proteins) have indicated that eosinophils should be considered as effector cells. We therefore investigated the possible release of granule proteins in response to signaling from ICAM-1 and its ligands. The concentrations of eosinophil cationic protein and eosinophil-derived neurotoxin in supernatants of eosinophils were significantly greater (p < 0.05) in the presence of recombinant soluble ICAM-1 than without it. These results suggest that signaling from ICAM-1 and its ligands might induce eosinophil activation and might be involved in degranulation of eosinophil granule proteins. In addition, reactive oxygen species generated by eosinophils have also been considered capable of causing airway injury at the inflamed focus. We examined the effect of recombinant soluble ICAM-1 and its ligands on eosinophil-induced radical oxygen products. Recombinant soluble ICAM-1 augmented eosinophil oxidative metabolism. It was concluded that signaling via adhesion molecules might play an important role in the pathogenesis of allergic inflammation through activation of eosinophils, such as through an increase in oxidative metabolism or degranulation of eosinophil granule proteins.
最近，人们发现黏附分子以及嗜酸性粒细胞在过敏性疾病的炎症过程中发挥着重要作用。我们的研究结果如下所示。哮喘患者嗜酸性粒细胞上黏附分子表达的特征，即黏附分子的高强度表达。PAF和RANTES可诱导黏附分子表达，此外，螨过敏原刺激的螨过敏性哮喘患者的单核细胞上清液以及重组IL-3、GM-CSF和IL-5的组合也可诱导黏附分子表达。支气管哮喘患者可溶性ICAM-1升高。此外，大量膜受体的存在以及细胞毒性分子（主要是颗粒碱性蛋白）的鉴定表明，嗜酸性粒细胞应被视为效应细胞。因此，我们研究了嗜酸性粒细胞是否可能响应ICAM-1及其配体的信号而释放颗粒蛋白。在存在重组可溶性ICAM-1的情况下，嗜酸性粒细胞上清液中嗜酸性粒细胞阳离子蛋白和嗜酸性粒细胞衍生神经毒素的浓度显著更高（p < 0.05）。这些结果表明，ICAM-1及其配体的信号可能诱导嗜酸性粒细胞活化，并可能参与嗜酸性粒细胞颗粒蛋白的脱颗粒。此外，嗜酸性粒细胞产生的活性氧也被认为能够在炎症灶处导致气道损伤。我们研究了重组可溶性ICAM-1及其配体对嗜酸性粒细胞诱导的活性氧产物的影响。重组可溶性ICAM-1增强了嗜酸性粒细胞的氧化代谢。得出的结论是，通过黏附分子的信号传导可能在过敏性炎症的发病机制中发挥重要作用，通过激活嗜酸性粒细胞，例如通过增加氧化代谢或嗜酸性粒细胞颗粒蛋白的脱颗粒。
