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首页> 美国卫生研究院文献>Infection and Immunity >α-23-Sialyltransferase Enhances Neisseria gonorrhoeae Survival during Experimental Murine Genital Tract Infection
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α-23-Sialyltransferase Enhances Neisseria gonorrhoeae Survival during Experimental Murine Genital Tract Infection

机译：α-23-唾液酸转移酶提高实验性小鼠生殖道感染过程中淋病奈瑟菌的存活率

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The addition of host-derived sialic acid to Neisseria gonorrhoeae lipooligosaccharide is hypothesized to be an important mechanism by which gonococci evade host innate defenses. This hypothesis is based primarily on in vitro assays of complement-mediated and phagocytic killing. Here we report that a nonpolar α-2,3-sialyltransferase (lst) mutant of N. gonorrhoeae was significantly attenuated in its capacity to colonize the lower genital tract of 17-β estradiol-treated female BALB/c mice during competitive infection with the wild-type strain. Genetic complementation of the lst mutation restored recovery of the mutant to wild-type levels. Studies with B10.D2-HCoH2dH2-T18c/OSN (C5-deficient) mice showed that attenuation of the lst mutant was not due to increased sensitivity to complement-mediated bacteriolysis, a result that is consistent with recently reported host restrictions in the complement cascade. However, Lst-deficient gonococci were killed more rapidly than sialylated wild-type gonococci following intraperitoneal injection into normal mice, which is consistent with sialylation conferring protection against killing by polymorphonuclear leukocytes (PMNs). As reported for human PMNs, sialylated gonococci were more resistant to killing by murine PMNs, and sialylation led to reduced association with and induction of a weaker respiratory burst in PMNs from estradiol-treated mice. In summary, these studies suggest sialylation confers a survival advantage to N. gonorrhoeae in mice by increasing resistance to PMN killing. This report is the first direct demonstration that α-2,3-sialyltransferase contributes to N. gonorrhoeae pathogenesis in an in vivo model. This study also validates the use of experimental murine infection to study certain aspects of gonococcal pathogenesis.
机译：淋病奈瑟氏球菌低聚糖中添加宿主衍生的唾液酸被认为是淋球菌逃避宿主固有防御的重要机制。该假设主要基于补体介导的吞噬杀伤的体外测定。在这里我们报告淋病奈瑟氏球菌的非极性α-2,3-唾液酸转移酶（lst）突变体在竞争性感染与17-β雌二醇处理的雌性BALB / c小鼠的下生殖道中的定殖能力显着减弱。野生型菌株。第一个突变的遗传互补将突变体的恢复恢复到野生型水平。 B10.D2-HC o H2 d H 2 -T18c / OSN（C5缺陷）小鼠的研究表明，第一个突变体的衰减这并不是由于对补体介导的溶菌作用的敏感性增加，这一结果与最近报道的宿主对补体级联反应的限制一致。然而，腹膜内注射到正常小鼠体内后，Lst缺陷型淋球菌比唾液酸化的野生型淋球菌更快地被杀死，这与唾液酸化赋予保护免受多形核白细胞（PMNs）杀伤的作用是一致的。如关于人类PMN的报道，唾液酸化的淋球菌对鼠类PMN的杀灭作用更具有抵抗力，而唾液酸化导致与雌二醇治疗的小鼠的PMN的缔合减少，并诱导了较弱的呼吸爆发。总之，这些研究表明，唾液酸化通过增加对PMN杀伤的抵抗力，使淋病奈瑟菌在小鼠中具有生存优势。该报道是在体内模型中α-2，3-唾液酸转移酶促成淋病奈瑟氏球菌发病机理的第一个直接证明。这项研究还验证了使用实验性鼠感染来研究淋球菌发病机理的某些方面。

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