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首页> 外文期刊>Infection and immunity >Phosphoethanolamine Substitution of Lipid A and Resistance of Neisseria gonorrhoeae to Cationic Antimicrobial Peptides and Complement-Mediated Killing by Normal Human Serum
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Phosphoethanolamine Substitution of Lipid A and Resistance of Neisseria gonorrhoeae to Cationic Antimicrobial Peptides and Complement-Mediated Killing by Normal Human Serum

机译：脂质A的磷酸乙醇胺取代和淋病奈瑟氏球菌对阳离子抗菌肽的抵抗以及正常人血清对补体介导的杀伤作用

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The capacity of Neisseria gonorrhoeae to cause disseminated gonococcal infection requires that such strains resist the bactericidal action of normal human serum. The bactericidal action of normal human serum against N. gonorrhoeae is mediated by the classical complement pathway through an antibody-dependent mechanism. The mechanism(s) by which certain strains of gonococci resist normal human serum is not fully understood, but alterations in lipooligosaccharide structure can affect such resistance. During an investigation of the biological significance of phosphoethanolamine extensions from lipooligosaccharide, we found that phosphoethanolamine substitutions from the heptose II group of the lipooligosaccharide β-chain did not impact levels of gonococcal (strain FA19) resistance to normal human serum or polymyxin B. However, loss of phosphoethanolamine substitution from the lipid A component of lipooligosaccharide, due to insertional inactivation of lptA, resulted in increased gonococcal susceptibility to polymyxin B, as reported previously for Neisseria meningitidis. In contrast to previous reports with N. meningitidis, loss of phosphoethanolamine attached to lipid A rendered strain FA19 susceptible to complement killing. Serum killing of the lptA mutant occurred through the classical complement pathway. Both serum and polymyxin B resistance as well as phosphoethanolamine decoration of lipid A were restored in the lptA-null mutant by complementation with wild-type lptA. Our results support a role for lipid A phosphoethanolamine substitutions in resistance of this strict human pathogen to innate host defenses.
机译：淋病奈瑟菌引起弥漫性淋球菌感染的能力要求这种菌株能抵抗正常人血清的杀菌作用。正常人血清对 N的杀菌作用。淋病由经典的补体途径通过抗体依赖性机制介导。某些淋球菌抵抗正常人血清的机制尚不完全清楚，但脂寡糖结构的改变会影响这种抵抗力。在对脂环寡糖中磷酸乙醇胺延伸的生物学意义进行的研究中，我们发现脂环寡糖β链的庚糖II组中的磷酸乙醇胺取代不会影响淋球菌（FA19株）对正常人血清或多粘菌素B的抗性水平。如先前针对脑膜炎奈瑟氏球菌报道的，由于 lptA 的插入失活，脂环寡糖的脂质A组分失去了磷酸乙醇胺取代，导致淋球菌对多粘菌素B的敏感性增加。与以前的 N报告相反。脑膜炎，与脂质A相连的磷酸乙醇胺的丢失使FA19菌株易于补体杀伤。通过经典补体途径杀死 lptA 突变体。通过补充野生型 lptA ，在 lptA -null突变体中恢复了血清和多粘菌素B的抗性以及脂质A的磷酸乙醇胺修饰。我们的结果支持脂质A磷酸乙醇胺取代在这种严格的人类病原体对先天宿主防御的抵抗中的作用。

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