Outer membrane vesicles (OMVs) are spherical bodies containing proteins and nucleic acids that are released by Gram-negative bacteria, including Borrelia burgdorferi, the causative agent of Lyme disease. The functional relationship between B. burgdorferi OMVs and host neuron homeostasis is not well understood. The objective of this study was to examine how B. burgdorferi OMVs impact the host cell environment. First, an in vitro model was established by co-culturing human BE2C neuroblastoma cells with B. burgdorferi B31. B. burgdorferi was able to invade BE2C cells within 24 h. Despite internalization, BE2C cell viability and levels of apoptosis remained unchanged, but resulted in dramatically increased production of MCP-1 and MCP-2 cytokines. Elevated secretion of MCP-1 has previously been associated with changes in oxidative stress. BE2C cell mitochondrial superoxides were reduced as early as 30 min after exposure to B. burgdorferi and OMVs. To rule out whether BE2C cell antioxidant response is the cause of decline in superoxides, superoxide dismutase 2 (SOD2) gene expression was assessed. SOD2 expression was reduced upon exposure to B. burgdorferi, suggesting that B. burgdorferi might be responsible for superoxide reduction. These results suggest that B. burgdorferi modulates cell antioxidant defense and immune system reaction in response to the bacterial infection. In summary, these results show that B. burgdorferi OMVs serve to directly counter superoxide production in BE2C neurons, thereby ‘priming’ the host environment to support B. burgdorferi colonization.

中文翻译：

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伯氏疏螺旋体外膜囊泡对宿主氧化应激反应的影响。


外膜囊泡 (OMV) 是含有蛋白质和核酸的球形体，由革兰氏阴性细菌释放，包括伯氏疏螺旋体（莱姆病的病原体）。伯氏疏螺旋体OMV 与宿主神经元稳态之间的功能关系尚不清楚。本研究的目的是研究伯氏疏螺旋体OMV 如何影响宿主细胞环境。首先，通过人BE2C神经母细胞瘤细胞与伯氏疏螺旋体B31共培养建立体外模型。伯氏疏螺旋体能够在 24 小时内侵入 BE2C 细胞。尽管内化，BE2C 细胞活力和细胞凋亡水平保持不变，但导致 MCP-1 和 MCP-2 细胞因子的产生显着增加。 MCP-1 分泌增加此前已被认为与氧化应激的变化有关。 BE2C 细胞线粒体超氧化物早在接触伯氏疏螺旋体和 OMV 后 30 分钟就减少了。为了排除 BE2C 细胞抗氧化反应是否是超氧化物下降的原因，我们评估了超氧化物歧化酶 2 (SOD2) 基因表达。 SOD2 表达在接触伯氏疏螺旋体后降低，表明伯氏疏螺旋体可能负责超氧化物的还原。这些结果表明伯氏疏螺旋体调节细胞抗氧化防御和免疫系统反应以应对细菌感染。总之，这些结果表明，伯氏疏螺旋体OMV 可直接对抗 BE2C 神经元中超氧化物的产生，从而“启动”宿主环境以支持伯氏疏螺旋体定植。