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首页> 外文期刊>The Journal of Experomental Medicine >Bacterial entry and intracellular processing of Neisseria gonorrhoeae in epithelial cells: immunomorphological evidence for alterations in the major outer membrane protein P.IB.
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Bacterial entry and intracellular processing of Neisseria gonorrhoeae in epithelial cells: immunomorphological evidence for alterations in the major outer membrane protein P.IB.

机译：淋病奈瑟菌在上皮细胞中的细菌进入和细胞内加工：主要外膜蛋白P.IB改变的免疫形态学证据。

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摘要

The fate of the major outer membrane protein of the gonococcus, P.IB, during the adherence, entry, and intracellular processing of the bacteria in infected epithelial cells was investigated using post-embedding immunoelectron microscopy. Various domains of the P.IB molecule were probed at different stages in the infection. These studies revealed that P.IB epitope exposure remained unaltered during the initial attachment of the bacteria to the host cells. In contrast, upon secondary attachment of the bacteria to the eukaryotic cells, apparent zones of adhesion were formed between the gonococci and the host cell membrane, which were characterized by loss of a defined P.IB epitope. These zones of adhesion with the altered P.IB immunoreactivity continued to exist and increased in number during cellular penetration, suggesting that they were essential to bacterial invasion into the eukaryotic cells. After bacterial entry, two classes of gonococci could be recognized; morphologically intact, P.IB-positive bacteria and disintegrated organisms that showed a change in, and, in a later stage, a complete loss of P.IB immunoreactivity. The intracellular alterations in the P.IB antigen could be prevented by treatment of the host cells with the lysosomotropic agent chloroquine. These observations point to a mechanism by which a subpopulation of intracellular gonococci can escape the epithelial cell defense by preventing or resisting exposure to host cell proteolytic activity.
机译：使用嵌入后免疫电子显微镜研究了在感染的上皮细胞中细菌的黏附，进入和细胞内加工过程中，淋球菌主要外膜蛋白P.IB的命运。在感染的不同阶段探查了P.IB分子的各个结构域。这些研究表明，在细菌最初附着于宿主细胞的过程中，P.IB表位的暴露保持不变。相反，当细菌继发于真核细胞上时，在淋球菌和宿主细胞膜之间形成了明显的粘附区，其特征在于丧失了确定的P.IB表位。这些具有改变的P.IB免疫反应性的粘附区继续存在并在细胞渗透期间数量增加，表明它们对于细菌侵入真核细胞至关重要。细菌进入后，可以识别出两类淋球菌。形态完整的P.IB阳性细菌和瓦解的生物体，其P.IB免疫反应性发生了变化，并在以后的阶段中完全丧失。 P.IB抗原的细胞内改变可以通过用溶溶同质剂氯喹处理宿主细胞来预防。这些观察结果指出了一种机制，通过该机制，细胞内淋球菌亚群可以通过预防或抵抗宿主细胞蛋白水解活性而逃脱上皮细胞防御。

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