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Interaction of Mycoplasma pneumoniae with HeLa cells.

机译:肺炎支原体与HeLa细胞的相互作用。

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摘要

The susceptibility of HeLa cells to Mycoplasma pneumoniae-induced injury was examined. Infections were initiated with relatively low mycoplasma doses, carried out in a culture medium incapable of supporting M. pneumoniae replication in the absence of host cells, and monitored for up to 10 days. Under these conditions, a time- and dose-dependent decline in the number of viable host cells compared with that of uninfected controls was observed. The effect of M. pneumoniae infection on host cell macromolecular synthesis was also evaluated. At high doses of infection, synthesis of both protein and RNA declined rapidly relative to that in control cells. At lower doses there was a biphasic response in protein synthesis, which was substantially lower than that in the uninfected control by day 1 postinfection, returned to control levels by day 4 postinfection, and was again less than that in control cells by day 7 postinfection. In contrast, no transient recovery was observed in RNA synthesis, which declined very gradually over 7 days in infected HeLa cells compared with that in uninfected control cells. The ability of HeLa cells to support the proliferation of M. pneumoniae under these experimental conditions was demonstrated by quantitation of mycoplasma CFU in the nonpermissive medium in the presence or absence of HeLa cells. A negligible increase in the number of M. pneumoniae was observed over 4 days when HeLa cells were absent, while CFU increased by almost 20-fold when M. pneumoniae was cultured in the presence of HeLa cells. The susceptibility and response in macromolecular synthesis in M. pneumoniae-infected HeLa cells differed from that recently described for a nontransformed culture of hamster trachea epithelial cells under the same experimental conditions (Y.-Y. Chen and D.C. Krause, Infect. Immun. 56: 570-576, 1988), underscoring the importance of the choice of host cell for in vitro modeling of M. pneumoniae pathogenesis.
机译:检查了HeLa细胞对肺炎支原体诱导的损伤的敏感性。用相对低的支原体剂量开始感染,在没有宿主细胞的情况下在不能支持肺炎支原体复制的培养基中进行感染,并监测长达10天。在这些条件下,与未感染的对照相比,观察到存活宿主细胞的数量呈时间和剂量依赖性下降。还评估了肺炎支原体感染对宿主细胞大分子合成的影响。在高剂量感染下,蛋白质和RNA的合成均相对于对照细胞迅速下降。在较低剂量下,蛋白质合成出现双相反应,到感染后第1天显着低于未感染对照的水平,感染后第4天恢复到对照水平,而感染后第7天再次低于对照细胞。相反,在RNA合成中未观察到瞬时恢复,与未感染的对照细胞相比,被感染的HeLa细胞在7天内逐渐下降。在这些实验条件下,HeLa细胞支持肺炎支原体增殖的能力通过定量在存在或不存在HeLa细胞的情况下,在非许可培养基中对支原体CFU的定量来证明。在没有HeLa细胞的情况下,经过4天的观察,肺炎支原体数量的增加可忽略不计,而在有HeLa细胞的情况下培养肺炎支原体时,CFU增加了近20倍。肺炎支原体感染的HeLa细胞中大分子合成的敏感性和响应不同于最近描述的在相同实验条件下仓鼠气管上皮细胞的非转化培养(Y.-Y. Chen和DC Krause,Infect。Immun.56) :570-576,1988),强调了选择宿主细胞对于肺炎支原体发病机理的体外建模的重要性。

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