Ibrahim A S, Filler S G, Ghannoum M A, Edwards J E
Department of Internal Medicine, Harbor-UCLA Medical Center, Torrance 90509.
J Infect Dis. 1993 Jun;167(6):1467-70. doi: 10.1093/infdis/167.6.1467.
Endothelial cells activated with interferon-gamma (IFN-gamma) have been shown to inhibit the replication of Toxoplasma gondii. To determine if this cytokine protects endothelial cells from damage by Candida albicans, human umbilical vein endothelial cells were pretreated with IFN-gamma and infected with C. albicans; endothelial cell damage was measured by the release of 51Cr. Pretreatment with IFN-gamma decreased the extent of endothelial cell injury caused by C. albicans by up to 100% +/- 8.2%. This diminution of endothelial cell damage was confirmed by scanning electron microscopy. The degree of protection was dependent on the concentration of IFN-gamma, with maximum protection occurring at 13 units/mL. Higher concentrations of IFN-gamma were toxic to the endothelial cells. Pretreating the endothelial cells with this cytokine had no effect on candidal germination and growth, suggesting that IFN-gamma stimulates endothelial cells to become resistant to or inhibit the action of candidal virulence factors.
γ干扰素(IFN-γ)激活的内皮细胞已被证明可抑制刚地弓形虫的复制。为了确定这种细胞因子是否能保护内皮细胞免受白色念珠菌的损伤,用人脐静脉内皮细胞先用IFN-γ预处理,然后感染白色念珠菌;通过释放51Cr来测量内皮细胞损伤。用IFN-γ预处理可使白色念珠菌引起的内皮细胞损伤程度降低达100%±8.2%。扫描电子显微镜证实了内皮细胞损伤的减轻。保护程度取决于IFN-γ的浓度,在13单位/毫升时出现最大保护作用。更高浓度的IFN-γ对内皮细胞有毒性。用这种细胞因子预处理内皮细胞对念珠菌的萌发和生长没有影响,这表明IFN-γ刺激内皮细胞对念珠菌毒力因子的作用产生抗性或抑制其作用。