Monack D, Falkow S
Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305-5124, USA.
Int J Med Microbiol. 2000 Mar;290(1):7-13. doi: 10.1016/S1438-4221(00)80096-X.
The comparison of common strategies used by bacterial pathogens to overcome host defenses provides us with the opportunity to analyze the biology of pathogenicity, as well as point out the unique interactions between a particular pathogen and its host. Here we compare and contrast apoptosis induced by three enteric pathogens, Salmonella, Shigella, and Yersinia. We point out that all three enteric pathogens induce apoptosis in macrophages in vitro, but the proposed mechanisms are quite different. Yersinia induces apoptosis by inhibiting the translocation of the transcriptional activator, NF-kappaB, into the nucleus, which results in the suppression of TNFalpha production; whereas Salmonella- and Shigella-induced apoptosis depend on the activation of caspase-1 (casp-1). The result of casp-1 activation is to induce apoptosis as well as to process the proinflammatory cytokines, pro-IL-1beta and pro-IL18 into their mature bioactive forms. Thus, in contrast to Yersinia, Salmonella and Shigella-induced apoptosis results in a proinflammatory cascade.
细菌病原体用于克服宿主防御的常见策略的比较，为我们提供了分析致病性生物学的机会，同时也指出了特定病原体与其宿主之间独特的相互作用。在这里，我们比较并对比了三种肠道病原体——沙门氏菌、志贺氏菌和耶尔森氏菌——诱导的细胞凋亡。我们指出，这三种肠道病原体在体外均能诱导巨噬细胞凋亡，但所提出的机制却大不相同。耶尔森氏菌通过抑制转录激活因子NF-κB向细胞核的转运来诱导细胞凋亡，这导致肿瘤坏死因子α（TNFα）的产生受到抑制；而沙门氏菌和志贺氏菌诱导的细胞凋亡则依赖于半胱天冬酶-1（casp-1）的激活。casp-1激活的结果是诱导细胞凋亡，同时将促炎细胞因子白细胞介素-1β前体（pro-IL-1β）和白细胞介素-18前体（pro-IL18）加工成其成熟的生物活性形式。因此，与耶尔森氏菌不同，沙门氏菌和志贺氏菌诱导的细胞凋亡会引发促炎级联反应。
