首页> 外文期刊>Infection and immunity >Interaction of Chlamydia psittaci reticulate bodies with mouse peritoneal macrophages.
【24h】

Interaction of Chlamydia psittaci reticulate bodies with mouse peritoneal macrophages.

机译:衣原体网状体与小鼠腹膜巨噬细胞的相互作用。

获取原文
           

摘要

Noninfectious reticulate bodies of Chlamydia psittaci are readily phagocytized by thioglycolate-elicited mouse peritoneal macrophages in monolayer culture. The internalized reticulate bodies are rapidly destroyed as indicated by a 60 to 70% decrease in trichloroacetic acid-precipitable radioisotopic counts in the macrophage pellet by 10 h and a concomitant increase of the trichloroacetic acid-soluble radiolabeled chlamydial nucleic acid in the cytoplasm. This intracellular destruction of reticulate bodies in macrophages is independent of the multiplicity of infection. Reticulate bodies at a high multiplicity of infection, up to 1,000:1, are also incapable of inducing immediate cytotoxicity in macrophages as evidenced by the lack of early release of the host cell-soluble cytoplasmic enzyme lactic dehydrogenase. Thus, it appears that the virulence factors for (i) initiation or maintenance of intracellular survival via circumvention of phagolysosome formation and (ii) host cell damage are either missing or not expressed by the RB form of this bacterium.
机译:衣原体的非感染性网状体很容易在单层培养中被巯基乙酸盐诱导的小鼠腹膜巨噬细胞吞噬。巨噬细胞沉淀中三氯乙酸可沉淀的放射性同位素计数下降60至70%,到10小时,胞质中三氯乙酸可溶的放射性标记衣原体核酸随之增加,表明内在的网状体被迅速破坏。巨噬细胞中网状体的这种细胞内破坏与感染的多样性无关。网状体在高达1000:1的高感染复数下也无法诱导巨噬细胞立即发生细胞毒性,这是由于缺乏宿主细胞可溶性胞质酶乳酸脱氢酶的早期释放所证明的。因此,似乎这种细菌的RB形式缺少(i)通过吞噬溶酶体形成的启动或维持细胞内存活和(ii)宿主细胞损伤的毒力因子。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号