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感染强毒肺炎支原体后器官培养中仓鼠气管代谢的改变。

Alterations in the metabolism of hamster tracheas in organ culture after infection by virulent Mycoplasma pneumoniae.

作者信息

Hu P C, Collier A M, Baseman J B

出版信息

Infect Immun. 1975 Apr;11(4):704-10. doi: 10.1128/iai.11.4.704-710.1975.

Abstract

Exposure of hamster tracheal rings in organ culture to virulent Mycoplasma pneumoniae organisms leads to alterations in macromolecular biosynthesis and metabolic activity of the respiratory epithelial cells. Avirulent organisms derived from the same parent strain do not produce these effects. During the course of infection by virulent mycoplasmas, tracheal rings show an initial increase in [14C]galactose uptake followed by a significant decline as infection progresses which is also accompanied by abnormal processing of galactose as evidenced by amounts of 14CO2 released. Parallel decreases in the rate of [3H]orotic acid and [3H]amino acid uptake are observed. Within 24 h after infection of tracheal rings by virulent mycoplasmas, inhibition of host cell ribonucleic acid and protien synthesis is evident. Ribonucleic acid synthesis in infected cells, analyzed by gel electrophoresis, is reduced by 80% at 48 h and is negligible by 96 h. The course of mycoplasma infection can be interrupted or reversed by erythromycin after the initial mycoplasma-host cell interaction since addition of erythromycin 24 h or earlier after infection prevents the onset of abnormal orotic acid uptake. However, 48 h after infection, rescue of host cells by erythromycin cannot occur and cytopathology becomes evident. These data suggest that mediation of host cell injury requires continued protein synthesis by attached mycoplasmas, and the primary effect of mycoplasma infection on tracheal organ culture may be at a transcriptional or translational level.

摘要

将仓鼠气管环置于器官培养中,使其暴露于强毒力肺炎支原体菌株会导致呼吸道上皮细胞的大分子生物合成和代谢活性发生改变。源自同一亲本菌株的无毒力菌株则不会产生这些影响。在被强毒力支原体感染的过程中,气管环对[14C]半乳糖的摄取最初会增加,随后随着感染的进展而显著下降,同时半乳糖的异常代谢也很明显,这可通过释放的14CO2量得以证明。观察到[3H]乳清酸和[3H]氨基酸摄取速率也相应下降。在气管环被强毒力支原体感染后的24小时内,宿主细胞核糖核酸和蛋白质合成受到明显抑制。通过凝胶电泳分析,感染细胞中的核糖核酸合成在48小时时减少80%,到96小时时可忽略不计。由于在感染后24小时或更早添加红霉素可防止异常乳清酸摄取的发生,因此在最初的支原体 - 宿主细胞相互作用后,红霉素可中断或逆转支原体感染的进程。然而,在感染48小时后,红霉素无法挽救宿主细胞,细胞病理学变化变得明显。这些数据表明,宿主细胞损伤的介导需要附着的支原体持续进行蛋白质合成,并且支原体感染对气管器官培养的主要影响可能发生在转录或翻译水平。

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