Yasuda M, Kokubu F, Izumi H, Matsukura S, Tokunaga H, Yamamoto T, Kuroiwa Y, Adachi M
Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Showa University.
Arerugi. 1995 Feb;44(2):100-3.
Bronchial asthma is characterized as a chronic inflammation of the airway that causes an infiltration of lymphocytes and eosinophils. Cell to cell interaction or cell to tissue interaction is essential for infiltration of eosinophils to underlying tissues. These phenomena are closely related to the expression of intercellular adhesion molecule-1 (ICAM-1). Inhalation of steroids, such as beclomethasone dipropionate, is commonly used to cure airway inflammation. In this study, we investigated the effect of cytokines on ICAM-1 expression on human bronchial epithelial cell lines, NCI-H292. Moreover, the effect of dexamethasone on ICAM-1 expression stimulated by IL-1 beta, TNF-alpha and IFN-gamma was observed. Treatment with IL-1 beta, TNF-alpha and IFN-gamma dose-dependently increased ICAM-1 expression on NCI-H292 cells. Inhibitory effects were exerted by dexamethasone on ICAM-1 expression in cells stimulated by IL-1 beta and IFN-gamma in a dose-dependent manner, but not in cells stimulated by TNF-alpha. These results suggest that the inhibition of ICAM-1 expression could be related to the pharmacological action of steroid drugs.
支气管哮喘的特征是气道慢性炎症，伴有淋巴细胞和嗜酸性粒细胞浸润。细胞间相互作用或细胞与组织间相互作用对于嗜酸性粒细胞浸润至下层组织至关重要。这些现象与细胞间黏附分子-1（ICAM-1）的表达密切相关。吸入类固醇，如二丙酸倍氯米松，常用于治疗气道炎症。在本研究中，我们调查了细胞因子对人支气管上皮细胞系NCI-H292上ICAM-1表达的影响。此外，还观察了地塞米松对由白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）刺激的ICAM-1表达的影响。用IL-1β、TNF-α和IFN-γ处理可使NCI-H292细胞上的ICAM-1表达呈剂量依赖性增加。地塞米松对由IL-1β和IFN-γ刺激的细胞中的ICAM-1表达具有剂量依赖性抑制作用，但对由TNF-α刺激的细胞则无此作用。这些结果表明，ICAM-1表达的抑制可能与类固醇药物的药理作用有关。
