A major catalase (KatB) that is required for resistance to H2O2 and phagocyte-mediated killing in Edwardsiella tarda
A major catalase (KatB) that is required for resistance to H2O2 and phagocyte-mediated killing in Edwardsiella tarda
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DOI：
10.1099/mic.0.26478-0
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发表时间：
2003-09-01
期刊：
影响因子：
2.8
通讯作者：
Leung, KY
中科院分区：
文献类型：
--
作者：
Rao, PSS;Yamada, Y;Leung, KY
迟缓爱德华氏菌可引起鱼的出血性败血症和包括人类在内的动物的胃肠道外感染。对吞噬细胞介导的杀伤的抵抗是ED的毒力因素之一。太迟了。作者先前使用TnPhoA转座子突变的研究表明，来自菌株PPD130/91的katB突变体的LD50值至少比野生型菌株高1.6对数。这些发现提示过氧化氢酶(KatB)参与了ED的发生。迟发性发病机制。在这项研究中，我们通过实验来表征KatB对ED的贡献。迟发性感染。Zymograph分析表明，22个ED。被研究的迟缓菌株根据它们在非变性聚丙烯酰胺凝胶中的迁移率表达三种不同类型的过氧化氢酶-过氧化物酶(Kat1-3)。在22例ED中有8例表达了主要的过氧化氢酶KatB(Kat1)。除AL9379外，常见于强毒株中。AL9379有一个突变的katB，它有一个碱基替换和一个可以翻译成过氧化氢酶基因中停止密码子的缺失。PPD130/91产生的KatB蛋白定位于胞浆和周质两个组分，并在不同生长期呈结构性表达。动力学研究表明，过氧化氢酶对过氧化氢和吞噬细胞介导的杀伤具有抵抗力。KatB突变体34在Gourami鱼体内的感染动力学研究表明，与野生型相比，它无法在富含吞噬细胞的器官中存活和复制，从而阻止了感染的传播。过氧化氢酶突变体的互补恢复了过氧化氢酶的产生，并导致对过氧化氢和吞噬细胞介导的杀伤的抗性增加，LD50值降低。本研究鉴定并鉴定了一个重要的过氧化氢酶基因(KatB)，该基因是ED抵抗过氧化氢和吞噬细胞介导的杀伤所必需的。太迟了。这些结果还表明，过氧化氢酶可能在ED中发挥毒力因子的作用。迟发性发病机制。
Edwardsiella tarda causes haemorrhagic septicaemia in fish and gastro- and extra-intestinal infections in animals including humans. Resistance to phagocyte-mediated killing is one of the virulence factors of Ed. tarda. The authors' previous studies using TnphoA transposon mutagenesis indicated that katB mutants derived from the strain PPD130/91 are at least 1.6 log higher in LD50 values than the wild-type strain. These findings suggest the involvement of catalase (KatB) in Ed. tarda pathogenesis. In this study, experiments were conducted to characterize the contribution of KatB to Ed. tarda infection. Zymographic analyses indicated that the 22 Ed. tarda strains examined expressed three different types of catalase-peroxidases (Kat1-3) based on their mobility in non-denaturing polyacrylamide gels. KatB (Kat1), the major catalase enzyme, was expressed in eight out of 22 Ed. tarda strains, and was commonly found in virulent strains except AL9379. AL9379 has a mutated katB, which has a base substitution and a deletion that translate into stop codons in the catalase gene. KatB produced by PPD130/91 was located in both periplasmic and cytoplasmic fractions and was constitutively expressed in various growth phases. Kinetics studies indicated that the catalase provided resistance to H2O2- and phagocyte-mediated killing. Infection kinetics studies of katB mutant 34 in gourami fish demonstrated its inability to survive and replicate in phagocyte-rich organs and this prevented the dissemination of infections when compared to the wild-type. Complementation of catalase mutants restored the production of catalase, and led to an increase in the resistance to H2O2- and phagocyte-mediated killing, and a decrease in LD50 values. This study has identified and characterized a major catalase gene (katB) that is required for resistance to H2O2- and phagocyte-mediated killing in Ed. tarda. The results also suggest that catalase may play a role as a virulence factor in Ed. tarda pathogenesis.