Lundberg B E, Wolf R E, Dinauer M C, Xu Y, Fang F C
Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA.
Infect Immun. 1999 Jan;67(1):436-8. doi: 10.1128/IAI.67.1.436-438.1999.
Salmonella typhimurium zwf mutants lacking glucose 6-phosphate dehydrogenase (G6PD) activity have increased susceptibility to reactive oxygen and nitrogen intermediates as well as attenuated virulence in mice. Abrogation of the phagocyte respiratory burst oxidase during experimental infection with zwf mutant Salmonella causes a prompt restoration of virulence, while inhibition of inducible nitric oxide synthase results in delayed lethality. These observations suggest that G6PD-dependent bacterial antioxidant defenses play an important pathogenic role during early salmonellosis and additionally may help to antagonize NO-dependent antimicrobial mechanisms later in the course of infection.
缺乏葡萄糖-6-磷酸脱氢酶(G6PD)活性的鼠伤寒沙门氏菌zwf突变体对活性氧和氮中间体的敏感性增加,并且在小鼠中的毒力减弱。在用zwf突变体沙门氏菌进行实验性感染期间,吞噬细胞呼吸爆发氧化酶的缺失导致毒力迅速恢复,而诱导型一氧化氮合酶的抑制则导致致死延迟。这些观察结果表明,G6PD依赖性细菌抗氧化防御在早期沙门氏菌病期间发挥重要的致病作用,并且在感染过程后期可能有助于对抗NO依赖性抗菌机制。