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首页> 外文期刊>Infection and immunity >Isolation and characterization of type III group B streptococcal mutants defective in biosynthesis of the type-specific antigen.
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Isolation and characterization of type III group B streptococcal mutants defective in biosynthesis of the type-specific antigen.

机译：在类型特异性抗原的生物合成中有缺陷的III型B组链球菌突变体的分离和鉴定。

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Four classes of mutants of type III group B streptococcus were isolated by serial subculture of the wild-type strain in the presence of type III-specific rabbit antiserum. Class I mutants no longer synthesized sialic acid but still elaborated the core antigen. Class II mutants maintained the ability to synthesize sialic acid but could not attach it to the core antigen. Class III mutants did not produce the core antigen but still synthesized intracellular sialic acid. Class IV mutants synthesized the complete antigen; however, only approximately 4% of the antigen synthesized was found associated with the cell wall peptidoglycan (in the wild-type strain greater than 85% of the antigen synthesized is covalently attached to the cell wall peptidoglycan), whereas greater than 90% of the antigen was secreted into the growth medium. Production of other components (CAMP factor, group B antigen, beta-hemolysin, neuraminidase) by these mutants appeared similar to those of the wild-type strain. Mouse lethality studies of these strains indicated that all four classes have greater than 3 log10-higher 50% lethal dose values than that of the wild-type strain. To understand the basis for this variation, the invasive ability of the wild-type strain and the sialic acid-deficient mutant strain M-10 (class I) was examined. Mice received 10(5) CFU of each organism; they were then sacrificed at various times postinoculation, and viable group B streptococci from different organs were enumerated. Mice were able to clear M-10 more efficiently, with greater than 80% of M-10 cells being phagocytized by macrophages within 1 h, whereas the wild-type strain was able to evade phagocytic killing and disseminate to other tissues. These data, therefore, strongly indicate that the sialic acid moiety greatly enhances the virulence of the type III antigen. In addition, the level of cell-associated type-specific antigen appears to contribute significantly to the pathogenicity of the organism.
机译：通过在III型特异性兔抗血清的存在下对野生型菌株进行连续继代培养，分离出四类III型B组链球菌突变体。 I类突变体不再合成唾液酸，但仍修饰了核心抗原。 II类突变体保持合成唾液酸的能力，但无法将其附着于核心抗原。 III类突变体不产生核心抗原，但仍合成细胞内唾液酸。 IV类突变体合成了完整的抗原;但是，仅发现约4％的合成抗原与细胞壁肽聚糖有关（在野生型菌株中，大于85％的合成抗原与细胞壁肽聚糖共价连接），而大于90％的抗原与细胞壁肽聚糖相关。抗原被分泌到生长培养基中。这些突变体产生的其他成分（CAMP因子，B组抗原，β-溶血素，神经氨酸酶）似乎与野生型菌株相似。这些菌株的小鼠致死性研究表明，所有四个类别的致死剂量值均比野生型菌株高3 log10-更高的50％致死剂量值。为了理解这种变异的基础，研究了野生型菌株和唾液酸缺乏突变株M-10（I类）的侵袭能力。小鼠接受每种生物体的10（5）CFU;然后在接种后的不同时间处死它们，并列举出来自不同器官的可行的B组链球菌。小鼠能够更有效地清除M-10，超过80％的M-10细胞在1小时内被巨噬细胞吞噬，而野生型菌株能够逃避吞噬细胞的杀死并传播到其他组织。因此，这些数据强烈表明唾液酸部分大大增强了III型抗原的毒性。另外，与细胞相关的类型特异性抗原的水平似乎对生物体的致病性有显着贡献。

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