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首页> 外文期刊>Infection and immunity >The (α2→8)-Linked Polysialic Acid Capsule and Lipooligosaccharide Structure Both Contribute to the Ability of Serogroup B Neisseria meningitidis To Resist the Bactericidal Activity of Normal Human Serum
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The (α2→8)-Linked Polysialic Acid Capsule and Lipooligosaccharide Structure Both Contribute to the Ability of Serogroup B Neisseria meningitidis To Resist the Bactericidal Activity of Normal Human Serum

机译：（α2→8）链接的聚唾液酸胶囊和脂寡糖结构都有助于血清脑膜炎奈瑟氏球菌血清B抵抗正常人血清的杀菌活性。

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摘要

The molecular basis for the resistance of serogroup BNeisseria meningitidis to the bactericidal activity of normal human sera (NHS) was examined with a NHS-resistant, invasive serogroup B meningococcal isolate and genetically and structurally defined capsule-, lipooligosaccharide (LOS)-, and sialylation-altered mutants of the wild-type strain. Expression of the (α2→8)-linked polysialic acid serogroup B capsule was essential for meningococcal resistance to NHS. The very NHS-sensitive phenotype of acapsular mutants (99.9 to 100% killed in 10, 25, and 50% NHS) was not rescued by complete LOS sialylation or changes in LOS structure. However, expression of the capsule was necessary but not sufficient for a fully NHS-resistant phenotype. In an encapsulated background, loss of LOS sialylation by interrupting the α2,3 sialyltransferase gene,lst, increased sensitivity to 50% NHS. In contrast, replacement of the lacto-N-neotetraose α-chain (Galβ1-4GlcNAcβ1-3Galβ1-4Glc) with glucose extensions (GlcN) in a galE mutant resulted in a strain resistant to killing by 50% NHS at all time points. Encapsulated meningococci expressing a Hep2(GlcNAc)→KDO2→lipid A LOS without an α-chain demonstrated enhanced sensitivity to 50% NHS (98% killed at 30 min) mediated through the antibody-dependent classical complement pathway. Encapsulated LOS mutants expressing truncated Hep2→KDO2→lipid A and KDO2→lipid A structures were also sensitive to 50% NHS (98 to 100% killed at 30 min) but, unlike the wild-type strain and mutants with larger oligosaccharide structures, they were killed by hypogammaglobulinemic sera. These data indicate that encapsulation is essential but that the LOS structure contributes to the ability of serogroup B N. meningitidis to resist the bactericidal activity of NHS.
机译：用NHS耐药，侵袭性B型脑膜炎球菌分离株以及基因和结构上确定的胶囊，检查了B群脑膜炎奈瑟氏球菌对正常人血清（NHS）杀菌活性的抗性的分子基础。野生型菌株的脂寡糖（LOS）和唾液酸化改变的突变体。 （α2→8）-连接的聚唾液酸B血清群胶囊的表达对于脑膜炎球菌对NHS的耐药性至关重要。完全的LOS唾液酸化或LOS结构的改变不能挽救高度对NHS敏感的荚膜突变体的表型（在10％，25％和50％的NHS中杀死了99.9至100％）。然而，胶囊的表达对于完全抗NHS的表型是必要的，但不足。在封闭的背景下，通过中断α2,3唾液酸转移酶基因 lst 导致LOS唾液酸化的丧失使对50％NHS的敏感性增加。相比之下，在 galE中用葡萄糖延伸片段（Glc N ）取代乳酸- N -新四糖α链（Galβ1-4GlcNAcβ1-3Galβ1-4Glc）。 突变体导致在所有时间点均能抵抗50％NHS杀伤的菌株。表达Hep 2 （GlcNAc）→KDO 2 →脂质A的包膜脑膜炎球菌对50％NHS的敏感性增强（在30分钟时98％被杀死）通过抗体依赖性经典补体途径介导。表达截短的Hep 2 →KDO 2 →脂质A和KDO 2 →脂质A结构的LOS突变体对50％NHS也敏感（98至30％时被杀死100％），但与野生型菌株和具有较大寡糖结构的突变体不同，它们被低γ-球蛋白血清杀死。这些数据表明包封是必不可少的，但是LOS结构有助于血清群B N的能力。脑膜炎可抵抗NHS的杀菌活性。

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