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Phospholipase A and the interaction of Rickettsia prowazekii and mouse fibroblasts (L-929 cells).

机译:磷脂酶A以及立氏立克次体和小鼠成纤维细胞(L-929细胞)的相互作用。

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摘要

L-929 cells were killed when approximately 50 viable Rickettsia prowazekii organisms per L-cell were centrifuged onto a monolayer. The glycerophospholipids of the L-cell were hydrolyzed to lysophosphatides and free fatty acids. Concomitantly, there was a loss of membrane integrity as shown by release of lactate dehydrogenase and 86Rb and permeability to trypan blue dye. No glycerophospholipid hydrolysis or cytotoxicity occurred when the rickettsiae were inactivated by heat, UV irradiation, N-ethylmaleimide, or metabolic inhibitors before their addition to the L-929 cells. On the other hand, treatment of the L929 cells with the cytoskeleton agents colchicine or cytochalasin B or with N-ethylmaleimide inhibited neither the phospholipase A activity nor the loss of membrane integrity. Cytochalasin B-treated cells could be damaged by even small numbers of rickettsiae. We suggest that this phospholipase A activity is used by the rickettsiae to escape from the phagosomes into the cytoplasm of host cells.
机译:将每个L细胞大约50种有活力的立克次氏体微生物离心到单层时,L-929细胞被杀死。 L细胞的甘油磷脂被水解为溶血磷脂和游离脂肪酸。伴随地,如乳酸脱氢酶和86Rb的释放以及对台盼蓝染料的渗透性所表明的,膜完整性的损失。当立克次体在加入L-929细胞之前通过加热,紫外线照射,N-乙基马来酰亚胺或代谢抑制剂失活时,未发生甘油磷脂水解或细胞毒性。另一方面,用细胞骨架剂秋水仙碱或细胞松弛素B或N-乙基马来酰亚胺处理L929细胞既不抑制磷脂酶A活性也不抑制膜完整性的丧失。细胞松弛素B处理的细胞甚至可能被少量立克次氏体破坏。我们建议立克次体使用这种磷脂酶A活性从吞噬体逃逸到宿主细胞的细胞质中。

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