Yuhas Y, Kaminsky E, Mor M, Ashkenazi S
Felsenstein Medical Research Center, Petah Tikva, Israel.
J Med Microbiol. 1996 Aug;45(2):97-102. doi: 10.1099/00222615-45-2-97.
Host mediators play an important role in the pathogenesis of shigellosis and Shiga toxin toxicity. Nitric oxide (NO) production in mouse peritoneal macrophages and in the macrophage J744 cell line in response to purified Shiga toxin and lipopolysaccharide (LPS) from Shigella flexneri were studied. Shiga toxin induced NO production in a dose-dependent manner up to 800 ng/ml. Detectable levels of NO were present as early as 4 h after induction and continued to increase during 72 h; Shiga toxin induced greater NO production with time than did LPS. Pre-treatment of Shiga toxin (400 ng/ml) or LPS (10 ng/ml) with polymyxin B, which inactivates LPS, reduced their ability to induce NO by 28% and 96%, respectively. Induction in the presence of anti-TNF alpha antibodies did not reduce the amount of NO in the supernate. These studies showed that Shiga toxin induces NO production in murine macrophages.
宿主介质在志贺氏菌病和志贺毒素毒性的发病机制中起重要作用。研究了小鼠腹腔巨噬细胞和巨噬细胞J744细胞系对纯化的志贺毒素和福氏志贺氏菌脂多糖（LPS）的反应中一氧化氮（NO）的产生。志贺毒素以剂量依赖方式诱导NO产生，直至800 ng/ml。诱导后4小时即可检测到NO水平，且在72小时内持续升高；志贺毒素随时间诱导产生的NO比LPS更多。用使LPS失活的多粘菌素B预处理志贺毒素（400 ng/ml）或LPS（10 ng/ml），分别使其诱导NO的能力降低28%和96%。在抗TNFα抗体存在下诱导并未减少上清液中NO的量。这些研究表明志贺毒素可诱导小鼠巨噬细胞产生NO。
