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Factors contributing to the reduced invasiveness of chlorine-injured Yersinia enterocolitica.

机译:导致氯损伤小肠结肠炎耶尔森氏菌侵袭性降低的因素。

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摘要

The invasion of epithelial cells in vitro and in vivo by chlorine-injured Yersinia enterocolitica was assessed by direct microscopic observations. These experiments showed that injury by chlorine inhibited invasiveness of virulent Y. enterocolitica. Two requirements appeared to be necessary for invasiveness: the organism must be viable and metabolically active, and the organism must have certain surface components to initiate engulfment. Inhibition of RNA synthesis by rifampin and protein synthesis by chloramphenicol, tetracycline, and spectinomycin inhibited the invasiveness but not the attachment of Y. enterocolitica to epithelial cells. Membrane preparations from untreated and antimicrobial-agent-treated Y. enterocolitica blocked the invasiveness of virulent Y. enterocolitica, whereas membranes from chlorinated cells were unable to block invasiveness. Chlorine did not change the hydrophobicity or surface charge of injured Y. enterocolitica. The results indicate that invasion was more than simple association of the bacterium with the epithelial cell and involved a specific trigger to stimulate engulfment.
机译:通过直接的显微镜观察来评估氯损伤的小肠结肠炎耶尔森氏菌在体外和体内对上皮细胞的侵袭。这些实验表明,氯损伤抑制了毒性肠小肠结肠炎耶尔森氏菌的侵袭性。入侵性似乎有两个要求:有机体必须具有活力和代谢活性,并且有机体必须具有一定的表面成分才能引发吞噬。利福平抑制RNA合成,氯霉素,四环素和大观霉素抑制蛋白合成,抑制了侵袭性,但不抑制小肠结肠炎耶尔森氏菌附着于上皮细胞。未经处理和用抗微生物剂处理过的小肠结肠炎耶尔森氏菌的膜制剂可阻止强毒小肠结肠炎耶尔森氏菌的侵袭,而氯化细胞的膜则无法阻止其侵袭。氯不会改变受伤的小肠结肠炎耶尔森氏菌的疏水性或表面电荷。结果表明,入侵不仅是细菌与上皮细胞的简单关联,而且还涉及刺激吞噬的特定触发因素。

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