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Macrophage secretion and the complement cleavage product C3a in the pathogenesis of infections by mycoplasmas and L-forms of bacteria and in immunity to these organisms.

机译:巨噬细胞分泌和补体切割产物C3a在支原体和L型细菌感染的发病机理中以及对这些生物体的免疫力方面。

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摘要

Mouse peritoneal macrophages in culture exposed to Mycoplasma pulmonis show marked biochemical changes. This micro-organism induces the release of hydrolytic enzymes from macrophages. The release is time- and dose-dependent and is not associated with loss of the cytoplasmic enzyme lactate dehydrogenase or any other sign of cell death. Secretory products of macrophages may play a role in the pathogenesis of chronic inflammatory responses elicited by mycoplasma infections. One of the products of activated macrophages is the complement cleavage product C3a. Purified C3a was incubated with M. hominis, M. pulmonis, Proteus mirabilis and an L-phase variant of this organism. All mycoplasmas and the L-phase variant were lysed by low concentrations of C3a, whereas the bacterial form of Pr. mirabilis was resistant.
机译:暴露于肺炎支原体的培养物中小鼠腹膜巨噬细胞显示出明显的生化变化。该微生物诱导巨噬细胞释放水解酶。释放是时间和剂量依赖性的,与细胞质酶乳酸脱氢酶的丧失或任何其他细胞死亡迹象无关。巨噬细胞的分泌产物可能在支原体感染引起的慢性炎症反应的发病机理中起作用。活化的巨噬细胞的产物之一是补体裂解产物C3a。将纯化的C3a与人型支原体,肺炎支原体,奇异变形杆菌和该生物的L期变体孵育。所有支原体和L期变体都被低浓度的C3a溶解,而细菌形式的Pr。奇异菌抗药。

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