首页> 外文期刊>The Journal of Infectious Diseases >Revisiting the importance of virulence determinant magA and its surrounding genes in Klebsiella pneumoniae causing pyogenic liver abscesses: exact role in serotype K1 capsule formation.
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Revisiting the importance of virulence determinant magA and its surrounding genes in Klebsiella pneumoniae causing pyogenic liver abscesses: exact role in serotype K1 capsule formation.

机译:回顾毒力决定因素magA及其周围基因在引起化脓性肝脓肿的肺炎克雷伯菌中的重要性:在血清型K1胶囊形成中的确切作用。

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BACKGROUND: Mucoviscosity-associated gene A (magA) is proposed to play a decisive role in the pathogenesis of liver abscesses due to Klebsiella pneumoniae. Although some investigators consider MagA to be a putative O-antigen ligase, it is also reportedly associated with the K1 antigen. METHODS: Using magA-positive serotype K1 K. pneumoniae STL43 isolated from a patient with liver abscess, we constructed 3 bacterial mutants by targeting genes within the same transcription unit, including magA, wcaG, and rfbP. The virulence of these mutants was determined by neutrophil phagocytosis and inoculation of mice. Transmission electron microscopy and Western blot analysis were used to define their surface polysaccharides. RESULTS: STL43 was resistant, and all 3 mutants were highly susceptible, to phagocytosis. None of the mutant strains caused death in mice at the lethal dose of STL43. In contrast to previous reports, transmission electron microscopy revealed that all 3 mutants were nonencapsulated. Analysis of surface polysaccharides revealed that all 3 mutants retained their O antigen but lost their K antigen/capsule. Furthermore, amino acid analysis showed that MagA shared a conserved domain of Wzy, the serotype-specific capsular polysaccharide polymerase. CONCLUSIONS: In accordance with the bacterial polysaccharide gene nomenclature (BPGN) scheme, MagA should be renamed Wzy(KpK1), the capsular polymerase specific to K. pneumoniae serotype K1.
机译:背景:粘膜粘度相关基因A(magA)被认为在肺炎克雷伯菌引起的肝脓肿的发病中起决定性作用。尽管一些研究人员认为MagA是推定的O抗原连接酶,但据报道它也与K1抗原相关。方法:使用从肝脓肿患者中分离出的magA阳性血清型K1肺炎克雷伯菌STL43,我们通过靶向同一转录单位内的基因(包括magA,wcaG和rfbP)构建了3个细菌突变体。这些突变体的毒性通过嗜中性粒细胞吞噬作用和小鼠接种来确定。使用透射电子显微镜和蛋白质印迹分析来定义其表面多糖。结果:STL43具有抗性,并且所有3个突变体均对吞噬作用高度敏感。在致死剂量的STL43下,没有任何突变株引起小鼠死亡。与以前的报告相反,透射电子显微镜显示所有3个突变体均未封装。表面多糖的分析表明,所有3个突变体均保留其O抗原,但丢失其K抗原/胶囊。此外,氨基酸分析表明,MagA共享Wzy的保守结构域,即血清型特异性荚膜多糖聚合酶。结论:根据细菌多糖基因命名法(BPGN),应将MagA重命名为Wzy(KpK1),这是肺炎克雷伯菌血清型K1特有的荚膜聚合酶。

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