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首页> 外文期刊>Infection and immunity >Role of Phosphoglucomutase of Bordetella bronchiseptica in Lipopolysaccharide Biosynthesis and Virulence
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Role of Phosphoglucomutase of Bordetella bronchiseptica in Lipopolysaccharide Biosynthesis and Virulence

机译：支气管败血波氏杆菌磷酸葡萄糖突变酶在脂多糖生物合成和毒力中的作用

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The phosphoglucomutase (PGM)-encoding gene of Bordetella bronchiseptica is required for lipopolysaccharide (LPS) biosynthesis. An insertion mutant of the wild-type B. bronchiseptica strain BB7865 which disrupted LPS biosynthesis was created and characterized (BB7865pgm). Genetic analysis of the mutated gene showed it shares high identity with PGM genes of various bacterial species and forms part of an operon which also encompasses the gene encoding phosphoglucose isomerase. Functional assays for PGM revealed that enzyme activity is expressed in bothbvg-positive and bvg-negative strains ofB. bronchiseptica and is substantially reduced in BB7865pgm. Complementation of the mutated PGM gene with that from BB7865 restored the wild-type condition for all phenotypes tested. The ability of the mutant BB7865pgm to survive within J774.A1 cells was significantly reduced at 2 h (40% reduction) and 24 h (56% reduction) postinfection. BB7865pgm was also significantly attenuated in its ability to survive in vivo following intranasal infection of mice, being effectively cleared from the lungs within 4 days, whereas the wild-type strain persisted at least 35 days. The activities of superoxide dismutase, urease, and acid phosphatase were unaffected in the PGM-deficient strain. In contrast, the inability to produce wild-type LPS resulted in a reduced bacterial resistance to oxidative stress and a higher susceptibility to the antimicrobial peptide cecropin P.
机译：脂多糖（LPS）的生物合成需要支气管败血博德特氏菌（Bordetella bronchiseptica）的磷酸化葡萄糖突变酶（PGM）编码基因。野生型 B的插入突变体。产生并鉴定了破坏LPS生物合成的支气管败血病菌BB7865（BB7865 pgm ）。对突变基因的遗传分析表明，它与各种细菌的PGM基因具有高度同一性，并构成操纵子的一部分，该操纵子还包含编码磷酸葡萄糖异构酶的基因。 PGM的功能分析表明， B的 bvg 阳性和 bvg 阴性菌株均表达酶活性。并在BB7865 pgm 中显着减少。突变的PGM基因与BB7865的互补，恢复了所有测试表型的野生型条件。感染后2小时（减少40％）和24小时（减少56％），突变体BB7865 pgm 在J774.A1细胞中存活的能力显着降低。 BB7865 pgm 在鼻内感染小鼠后体内存活能力也显着减弱，在4天内有效地从肺中清除，而野生型菌株持续至少35天。在PGM缺陷菌株中，超氧化物歧化酶，脲酶和酸性磷酸酶的活性不受影响。相反，无法产生野生型LPS导致细菌对氧化应激的抵抗力降低，并且对抗菌肽天蚕素P的敏感性更高。

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