Santucci L A, Gutierrez P L, Silverman D J
Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore.
Infect Immun. 1992 Dec;60(12):5113-8. doi: 10.1128/iai.60.12.5113-5118.1992.
Human endothelial cells infected with Rickettsia rickettsii, the etiological agent of Rocky Mountain spotted fever, undergo striking morphological changes to the endoplasmic reticulum-outer nuclear envelope complex. These changes are accompanied by concurrent accumulation of intracellular peroxides. Both of these findings are consistent with the notion that cells undergo some form of oxidative stress. Since oxidant injury is often initiated or mediated through oxygen radicals, we examined superoxide radical generation when endothelial cells were exposed to R. rickettsii. We also examined the levels of superoxide dismutase, an enzyme induced in response to increased superoxide formation. The levels of both superoxide and superoxide dismutase increased when endothelial cells were exposed to R. rickettsii. These results, together with our previous findings, support our hypothesis that cells infected by this intracellular bacterium experience oxidant-mediated injury that may eventually contribute to cell death.
感染落基山斑疹热病原体立氏立克次体的人内皮细胞,其内质网 - 外核膜复合体发生显著形态变化。这些变化伴随着细胞内过氧化物的同时积累。这两个发现都与细胞经历某种形式氧化应激的观点一致。由于氧化损伤通常由氧自由基引发或介导,我们检测了内皮细胞暴露于立氏立克次体时超氧阴离子自由基的产生情况。我们还检测了超氧化物歧化酶的水平,该酶是因超氧形成增加而诱导产生的一种酶。当内皮细胞暴露于立氏立克次体时,超氧和超氧化物歧化酶的水平均升高。这些结果与我们之前的发现一起,支持了我们的假设,即被这种细胞内细菌感染的细胞会经历氧化介导的损伤,最终可能导致细胞死亡。