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首页> 外文期刊>Microbes and infection >Differential contribution of sodC1 and sodC2 to intracellular survival and pathogenicity of Salmonella enterica serovar Choleraesuis
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Differential contribution of sodC1 and sodC2 to intracellular survival and pathogenicity of Salmonella enterica serovar Choleraesuis

机译：sodC1和sodC2对肠炎沙门氏菌血清霍乱弧菌的细胞内存活和致病性的不同贡献

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摘要

Several of the most virulent Salmonella enterica strains possess two genes encoding periplasmic Cu,Zn superoxide dismutase, sodC1 and sodC2, located on a lambdoid prophage and on the chromosome, respectively. These genes contribute to Salmonella virulence by protecting bacteria from superoxide generated by the host's phagocytes. To investigate the respective contributions of sodC1 and sodC2 to the virulence of a clinical isolate of Salmonella enterica serovar Choleraesuis (S. choleraesuis), we have analyzed both the intracellular survival of wild type and sodC mutant strains within J774 macrophages and Caco-2 cells, and their ability to proliferate in intraperitoneally-infected mice in competition assays. In agreement with previous studies, mutant strains lacking one or both sodC genes were equally impaired in their ability to survive within activated macrophages. However, when macrophage killing experiments were carried out with non-opsonized bacteria, sodC2 contributed to intracellular survival more than sodC1, indicating that changes in the pathways of bacterial uptake can modify the relative role of the two sodC genes. More unexpectedly, we have found that the ability of S. choleraesuis to survive within Caco-2 cells was severely affected by inactivation of sodC genes, sodC2 being more important than sodC1. As Caco-2 cells actively produce superoxide, this suggests that oxygen radical production by colonic cells has a role in controlling proliferation of facultative intracellular bacteria. Mouse infection studies confirmed that, in the S. choleraesuis strain under investigation, both sodC genes are required to confer full virulence, sodC2 contributing slightly more than sodC1 to Salmonella pathogenesis. Our findings contrast with the results of other studies carried out in S. enterica serovar Typhimurium and suggest that the relative contributions of sodC1 and sodC2 to host-pathogen interactive biology may vary depending on the Salmonella serovar or strain. (c) 2005 Elsevier SAS. All rights reserved.
机译：几个最具毒性的肠炎沙门氏菌菌株分别具有两个编码周质Cu，Zn超氧化物歧化酶，sodC1和sodC2的基因，分别位于lambdoid噬菌体和染色体上。这些基因通过保护细菌免于宿主吞噬细胞产生的超氧化物而有助于沙门氏菌的致病性。为了研究sodC1和sodC2对肠炎沙门氏菌霍乱沙门氏菌（S. choleraesuis）临床分离株的毒力的贡献，我们分析了J774巨噬细胞和Caco-2细胞内野生型和sodC突变株的细胞内存活，以及它们在竞争试验中在腹膜内感染小鼠中的增殖能力。与先前的研究一致，缺少一个或两个sodC基因的突变菌株在活化的巨噬细胞中存活的能力也同样受到损害。但是，当用非调理细菌进行巨噬细胞杀灭实验时，sodC2对细胞内存活的贡献要大于sodC1，这表明细菌摄取途径的改变可以修饰两个sodC基因的相对作用。更出乎意料的是，我们发现霍乱链球菌在Caco-2细胞中生存的能力受到sodC基因失活的严重影响，其中sodC2比sodC1更重要。由于Caco-2细胞活跃地产生超氧化物，这表明结肠细胞产生氧自由基在控制兼性细胞内细菌的增殖中具有作用。小鼠感染研究证实，在所研究的霍乱链球菌菌株中，两个sodC基因都必须具有完全的毒力，而sodC2在沙门氏菌发病中的作用比sodC1略强。我们的发现与在鼠伤寒沙门氏菌鼠伤寒沙门氏菌中进行的其他研究结果相反，并表明sodC1和sodC2对宿主-病原体相互作用生物学的相对贡献可能会随沙门氏菌血清型或菌株而变化。 （c）2005 Elsevier SAS。版权所有。

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