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首页> 外文期刊>Infection and immunity >The Salmonella virulence plasmid enhances Salmonella-induced lysis of macrophages and influences inflammatory responses.
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The Salmonella virulence plasmid enhances Salmonella-induced lysis of macrophages and influences inflammatory responses.

机译：沙门氏菌毒力质粒增强了巨噬细胞的裂解裂解，影响炎症反应。

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The Salmonella dublin virulence plasmid mediates systemic infection in mice and cattle. Here, we analyze the interaction between wild-type and plasmid-cured Salmonella strains with phagocytes in vitro and in vivo. The intracellular recovery of S. dublin from murine peritoneal and bovine alveolar macrophages cultured in the presence of gentamicin in vitro was not related to virulence plasmid carriage. However, the virulence plasmid increased the lytic activity of S. dublin, Salmonella typhimurium, and Salmonella choleraesuis for resident or activated mouse peritoneal macrophages. Lysis was not mediated by spv genes and was abolished by cytochalasin D treatment. Peritoneal and splenic macrophages were isolated from mice 4 days after intraperitoneal infection with wild-type or plasmid-cured S. dublin strains. The wild-type strain was recovered in significantly higher numbers than the plasmid-cured strain. However, the intracellular killing rates of such cells cultured in vitro for both S. dublin strains were not significantly different. Four days after infection, there was a lower increase of phagocyte numbers in the peritoneal cavities and spleens of mice infected with the wild-type strain compared with the plasmid-cured strain. The virulence plasmid influenced the survival of macrophages in vitro following infection in vivo as assessed by microscopy. Cells from mice infected with the plasmid-cured strain survived better than those from mice infected with the wild-type strain. This is the first report demonstrating an effect of the virulence plasmid on the interaction of Salmonella strains with macrophages. Plasmid-mediated macrophage dysfunction could influence the recruitment and/or the activation of phagocytic cells and consequently the net growth of Salmonella strains during infection.
机译：沙门氏菌都柏林毒力质粒介导小鼠和牛的全身感染。在这里，我们分析野生型和质粒固化的沙门氏菌在体外和体内吞噬细胞的相互作用。在体外庆大霉素存在下培养的鼠腹膜和牛肺泡巨噬细胞的细胞内恢复与毒力质粒携带无关。然而，毒力质粒增加了S. dublin，沙门氏菌毒蕈尿和沙门氏菌的裂变活性，用于居民或活化的小鼠腹膜巨噬细胞。裂解未被SPV基因介导，并通过细胞蛋白D治疗废除。腹膜和脾巨噬细胞与腹膜内感染后4天与野生型或质粒固化的S.都柏林菌株分离出腹膜和脾巨噬细胞。野生型菌株在比质粒固化的菌株的数量显着更高。然而，对于都柏林菌株体外培养的这种细胞的细胞内杀伤率并没有显着差异。感染后四天，与质粒固化菌株相比，腹膜腔体中骨骼腔内吞噬细胞数量较低，小鼠的脾脏增加。毒力质粒影响巨噬细胞在体外巨噬细胞的存活率，如通过显微镜评估的体内感染。来自细胞质固化的菌株的小鼠的细胞优于来自野生型菌株的小鼠的小鼠的生存。这是第一份报告，证明了毒力质粒对巨噬细胞的沙门氏菌菌株相互作用的影响。质粒介导的巨噬细胞功能障碍可能影响植物细胞的招生和/或激活吞噬细胞，并因此在感染过程中培养的净生长。

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