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Influence of protein synthesis inhibitors on regulation of extent of O-acetylation of gonococcal peptidoglycan.

机译:蛋白质合成抑制剂对淋球菌肽聚糖O-乙酰化程度的调节。

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The effects of protein synthesis inhibitors on the extent of O-acetylation of Neisseria gonorrhoeae peptidoglycan (PG) and on the resistance of PG to degradation by human PG hydrolases were examined. Addition of chloramphenicol, tetracycline, and streptomycin (in amounts equal to approximately twice their respective MICs) rapidly increased the level of O-acetylation of [3H]glucosamine-labeled N. gonorrhoeae FA19 PG from 46% to about 70% and simultaneously enhanced the resistance of the PG to degradation by human polymorphonuclear leukocyte lysozyme. Entry into the stationary phase also enhanced O-acetylation of FA19 PG, but neither protein synthesis inhibitors nor the stationary phase had a detectable effect on the O-acetyl-deficient, lysozyme-sensitive PG of N. gonorrhoeae RD5. Mild alkali treatment of PG derived from chloramphenicol-treated FA19 specifically removed O-acetyl groups and simultaneously reduced the extents of O-acetylation and polymorphonuclear leukocyte lysozyme resistance to the level of RD5 PG, suggesting that the O-acetyl substituents were solely responsible for the increased PG hydrolase resistance of PG from chloramphenicol-treated FA19. Pulse-chase experiments indicated that the drug-mediated enhancement of O-acetylation was limited to newly assembled PG. In summary, conditions favoring unbalanced macromolecular synthesis and bacteriostasis increased the level of O-acetylation and the PG hydrolase resistance of gonococcal PG. Similar conditions encountered by gonococci in vivo might potentiate the pathobiological consequences of PG-host interactions.
机译:研究了蛋白质合成抑制剂对淋病奈瑟氏球菌肽聚糖(PG)的O-乙酰化程度以及PG对人PG水解酶降解的抗性的影响。氯霉素,四环素和链霉素的添加(大约等于其各自MIC的两倍)可将[3H]葡糖胺标记的淋病奈瑟氏球菌FA19 PG的O-乙酰化水平迅速提高,从46%增至约70%,同时增强PG对人多形核白细胞溶菌酶降解的抗性。进入固定相还可以增强FA19 PG的O-乙酰化作用,但是蛋白质合成抑制剂和固定相均不能对淋病奈瑟氏球菌RD5的O-乙酰基缺乏,溶菌酶敏感的PG产生可检测的影响。对用氯霉素处理过的FA19衍生的PG进行轻度碱处理会特别去除O-乙酰基,同时将O-乙酰化和多形核白细胞溶菌酶的抗性程度降低至RD5 PG的水平,这表明O-乙酰基取代基完全负责增强了氯霉素处理的FA19对PG的PG水解酶的抗性。脉冲追踪实验表明,药物介导的O-乙酰化增强仅限于新组装的PG。总之,有利于大分子合成和抑菌的不平衡条件增加了淋球菌PG的O-乙酰化水平和PG水解酶抗性。淋球菌在体内遇到的类似条件可能会增强PG-宿主相互作用的病理生物学后果。

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