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首页> 美国卫生研究院文献>Infection and Immunity >Superoxide Dismutase-Deficient Mutants of Helicobacter pylori Are Hypersensitive to Oxidative Stress and Defective in Host Colonization
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Superoxide Dismutase-Deficient Mutants of Helicobacter pylori Are Hypersensitive to Oxidative Stress and Defective in Host Colonization

机译：幽门螺杆菌的超氧化物歧化酶缺陷型突变体对氧化应激高度敏感并且在宿主定殖中有缺陷。

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Superoxide dismutase (SOD) is a nearly ubiquitous enzyme among organisms that are exposed to oxic environments. The single SOD of Helicobacter pylori, encoded by the sodB gene, has been suspected to be a virulence factor for this pathogenic microaerophile, but mutations in this gene have not been reported previously. We have isolated mutants with interruptions in the sodB gene and have characterized them with respect to their response to oxidative stress and ability to colonize the mouse stomach. The sodB mutants are devoid of SOD activity, based on activity staining in nondenaturing gels and quantitative assays of cell extracts. Though wild-type H. pylori is microaerophilic, the mutants are even more sensitive to O2 for both growth and viability. While the wild-type strain is routinely grown at 12% O2, growth of the mutant strains is severely inhibited at above 5 to 6% O2. The effect of O2 on viability was determined by subjecting nongrowing cells to atmospheric levels of O2 and plating for survivors at 2-h time intervals. Wild-type cell viability dropped by about 1 order of magnitude after 6 h, while viability of the sodB mutant decreased by more than 6 orders of magnitude at the same time point. The mutants are also more sensitive to H2O2, and this sensitivity is exacerbated by increased O2 concentrations. Since oxidative stress has been correlated with DNA damage, the frequency of spontaneous mutation to rifampin resistance was studied. The frequency of mutagenesis of an sodB mutant strain is about 15-fold greater than that of the wild-type strain. In the mouse colonization model, only 1 out of 23 mice inoculated with an SOD-deficient mutant of a mouse-adapted strain became H. pylori positive, while 15 out of 17 mice inoculated with the wild-type strain were shown to harbor the organism. Therefore, SOD is a virulence factor which affects the ability of this organism to colonize the mouse stomach and is important for the growth and survival of H. pylori under conditions of oxidative stress.
机译：在暴露于有氧环境的生物中，超氧化物歧化酶（SOD）是几乎普遍存在的酶。有人怀疑由sodB基因编码的幽门螺杆菌的单一SOD是这种致病性微需氧菌的致病因子，但该基因的突变以前尚未见报道。我们已分离出sodB基因中断的突变体，并对它们对氧化应激的反应和定居小鼠胃的能力进行了表征。基于非变性凝胶中的活性染色和细胞提取物的定量分析，sodB突变体没有SOD活性。尽管野生型幽门螺杆菌是微需氧的，但突变体对O2的生长和生存力甚至更加敏感。尽管野生型菌株通常在12％的O2下生长，但突变型菌株的生长却在高于5％至6％的O2下受到严重抑制。通过使未生长的细胞经受大气中的O2浓度并以2小时的时间间隔接种给存活者，来确定O2对生存力的影响。 6小时后，野生型细胞的活力下降了大约1个数量级，而sodB突变体的活力在同一时间点下降了6个数量级以上。突变体对H2O2也更加敏感，而O2浓度的增加会加剧这种敏感性。由于氧化应激与DNA损伤相关，因此研究了自发突变对利福平耐药的频率。 sodB突变菌株的诱变频率比野生型菌株诱变的频率高约15倍。在小鼠定殖模型中，接种了小鼠适应性菌株的SOD缺陷型突变体的23只小鼠中只有1例成为幽门螺杆菌阳性，而野生型菌株的17只小鼠中有15只具有该菌。 。因此，SOD是一种毒性因子，会影响该生物体在小鼠胃中定植的能力，并且对于氧化应激条件下幽门螺杆菌的生长和存活至关重要。

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