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首页> 外文期刊>Infection and immunity >Interaction of Mycoplasma arthritidis and Other Mycoplasmas with Murine Peritoneal Macrophages
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Interaction of Mycoplasma arthritidis and Other Mycoplasmas with Murine Peritoneal Macrophages

机译：关节炎支原体和其他支原体与小鼠腹膜巨噬细胞的相互作用

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摘要

Neither mouse nor rat peritoneal macrophages were able to kill Mycoplasma arthritidis to any observable degree in the absence of specific hyperimmune rabbit antiserum. Although convalescent mouse and rat serum were somewhat inhibitory to M. arthritidis in the absence of macrophages, these sera did not promote active phagocytosis by peritoneal macrophages. In fact, the macrophages appeared to protect the mycoplasmas against the inhibitory effects of the antisera by stimulating their growth. Hyperimmune rabbit antiserum against M. arthritidis initiated phagocytic action and resulted in a 50-fold decrease in numbers of viable mycoplasmas by 6 h. In contrast with M. arthritidis, M. pulmonis rapidly adsorbed to the surface of peritoneal macrophages. Upon addition of specific rabbit antiserum, a rapid decrease in viable organisms occurred, and a more complete destruction of organisms ensued in comparison with M. arthritidis. M. gallinarum, as with M. arthritidis, did not adsorb to the macrophages to any great extent. Phagocytic action was observed only in the presence of homologous rabbit antiserum and was not marked until after 6 h of incubation.
机译：在缺乏特异性超免疫兔抗血清的情况下，小鼠和大鼠腹膜巨噬细胞均无法杀死关节炎支原体。尽管恢复期的小鼠和大鼠血清对 M有一定的抑制作用。在没有巨噬细胞的关节炎中，这些血清不能促进腹膜巨噬细胞的主动吞噬作用。实际上，巨噬细胞似乎通过刺激支原体的生长来保护支原体免受抗血清的抑制作用。针对 M的超免疫兔抗血清。关节炎引发吞噬作用，导致6h内存活的支原体数量减少了50倍。与 M相反。关节炎，肺炎支原体迅速吸附到腹膜巨噬细胞表面。与 M相比，添加特定的兔抗血清后，活菌迅速减少，并随后彻底破坏了生物。关节炎。 M. gallinarum ，与 M。关节炎在很大程度上没有吸附到巨噬细胞上。仅在同源兔抗血清的存在下才观察到吞噬作用，并且直到孵育6小时才被标记。

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