ALTERATIONS IN METABOLISM OF HAMSTER TRACHEAS IN ORGAN-CULTURE AFTER INFECTION BY VIRULENT MYCOPLASMA-PNEUMONIAE

ALTERATIONS IN METABOLISM OF HAMSTER TRACHEAS IN ORGAN-CULTURE AFTER INFECTION BY VIRULENT MYCOPLASMA-PNEUMONIAE
复制标题

DOI:
10.1128/iai.11.4.704-710.1975
复制
发表时间:
1975-01-01
影响因子:
3.1
通讯作者:
BASEMAN, JB
BASEMAN, JB
中科院分区:
医学2区
文献类型:
--
作者:
HU, PC;COLLIER, AM;BASEMAN, JB

文献摘要

被引文献

相似文献

器官培养中仓鼠气管环暴露于毒性肺炎支原体微生物导致呼吸道上皮细胞大分子生物合成和代谢活性改变。来自同一亲本菌株的无毒微生物不产生这些效应。在毒性支原体感染过程中,气管环显示[14C]半乳糖摄取最初增加,随后随着感染进展而显著下降,这也伴随着半乳糖的异常加工,如释放的14CO2量所证明的。观察到[3H]乳清酸和[3H]氨基酸摄取速率平行降低。在24小时内感染气管环的毒性支原体,抑制宿主细胞核糖核酸和蛋白质的合成是明显的。通过凝胶电泳分析,感染细胞中的核糖核酸合成在48小时减少80%,到96小时可以忽略不计。在最初的支原体与宿主细胞相互作用后,红霉素可以中断或逆转支原体感染的过程,因为在感染后24小时或更早添加红霉素可以防止异常乳清酸摄入的发生。然而,感染后48小时,红霉素不能拯救宿主细胞,细胞病理学变得明显。这些数据表明,介导的宿主细胞损伤需要持续的蛋白质合成附着支原体,支原体感染气管器官培养的主要影响可能是在转录或翻译水平。
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.