Ohrui T, Yamaya M, Sekizawa K, Yamada N, Suzuki T, Terajima M, Okinaga S, Sasaki H
Department of Geriatric Medicine, Tohoku University School of Medicine, Sendai 980, Japan.
Am J Respir Crit Care Med. 1998 Jul;158(1):241-8. doi: 10.1164/ajrccm.158.1.9607117.
To investigate whether rhinovirus infection impairs epithelial barrier functions, human rhinovirus 14 (HRV-14) was infected to primary cultures of human tracheal epithelial cells and experiments were performed on Day 2 after HRV-14 infection. Hydrogen peroxide (H2O2; 3 x 10(-)4 M) increased electrical conductance (G) across the epithelial cell sheet measured with Ussing's chamber methods. Exposure of the epithelial cells to HRV-14 had no effect on H2O2-induced increases in G and [3H]mannitol flux through the cultured epithelium in the control condition, but it markedly potentiated H2O2- induced increases in both parameters in IL-1beta (100 U/ml) pretreated condition. However, pretreatment with TNF-alpha (100 U/ml) was without effect. IL-1beta enhanced the intercellular adhesion molecule-1 (ICAM-1) expression assessed by immunohistochemical analysis and susceptibility of epithelial cells to HRV-14 infection. An antibody to ICAM-1 inhibited HRV-14 infection of epithelial cells and abolished H2O2-induced increases in G and [3H]mannitol flux in IL-1beta-pretreated epithelial cells with HRV-14 infection. These results suggest that rhinovirus infection may reduce barrier functions in the airway epithelium in association with upregulation of ICAM-1 expression.
为了研究鼻病毒感染是否会损害上皮屏障功能,将人鼻病毒14型(HRV-14)感染人气管上皮细胞原代培养物,并在HRV-14感染后第2天进行实验。过氧化氢(H2O2;3×10(-)4 M)通过尤斯灌流小室法测量,增加了跨上皮细胞片的电导(G)。在对照条件下,将上皮细胞暴露于HRV-14对H2O2诱导的G增加和[3H]甘露醇通过培养上皮的通量没有影响,但在白细胞介素-1β(IL-1β;100 U/ml)预处理条件下,它显著增强了H2O2诱导的这两个参数的增加。然而,用肿瘤坏死因子-α(TNF-α;100 U/ml)预处理没有效果。IL-1β通过免疫组织化学分析评估增强了细胞间黏附分子-1(ICAM-1)的表达以及上皮细胞对HRV-14感染的易感性。抗ICAM-1抗体抑制了上皮细胞的HRV-14感染,并消除了H2O2诱导的IL-1β预处理的感染HRV-14的上皮细胞中G和[3H]甘露醇通量的增加。这些结果表明,鼻病毒感染可能与ICAM-1表达上调相关,降低气道上皮的屏障功能。