Yunnan Province Key Laboratory for Tropical Infectious Diseases in Universities, Kunming 650500, China; Department of Microbiology and Immunology, Kunming Medical University, Kunming 650500, China.
Yunnan Province Key Laboratory for Tropical Infectious Diseases in Universities, Kunming 650500, China; The Institute for Tropical Medicine, Kunming Medical University, Kunming 650500, China; Yunnan Province Integrative Innovation Center for Public Health, Diseases Prevention and Control, Kunming Medical University, Kunming 650500, China; Yunnan Demonstration Base of International Science and Technology Cooperation for Tropical Diseases, Kunming 650500, China; Department of Biochemistry and Molecular Biology, Kunming Medical University, Kunming 650500, China.
Microb Pathog. 2017 Oct;111:174-181. doi: 10.1016/j.micpath.2017.08.036. Epub 2017 Sep 1.
Lyme neuroborreliosis is a nervous system infectious disease caused by Borrelia burgdorferi (B. burgdorferi). It has been demonstrated that cytokines induced by B. burgdorferi are related to Lyme neuroborreliosis. Microglia is known as a key player in the immune responses that occur within the central nervous system. In response to inflammation, it will be activated and generate cytokines and chemokines. Experiments in vitro cells have showed that B. Burgdorferi membrane protein A (BmpA), a major immunogen of B. Burgdorferi, could induce Lyme arthritis and stimulate human and murine lymphocytes to produce inflammatory cytokines. In our study, the murine microglia BV2 cell line was used as a cell model to explore the stimulating effects of recombinant BmpA (rBmpA); Chemokine chip, ELISA and QPCR technology were used to measure the production of chemokines from microglial cells stimulated by rBmpA. Compared with the negative control group, CXCL2, CCL22, and CCL5 concentrations in the cell supernatant increased significantly after the rBmpA stimulation; the concentration of these chemokines increased with rBmpA concentration increasing; the mRNA expression levels of chemokines (CXCL2, CCL22, and CCL5) in murine BV2 cells increased significantly with 10 μg/mL and 20 μg/mL rBmpA stimulation; CXCL13 was not change after the rBmpA stimulation. Our study shows that chemokines, such as CXCL2, CCL22, and CCL5 were up-regulated by the rBmpA in the BV2 cells. The production of chemokines in Lyme neuroborreliosis may be mainly from microglia cells and the rBmpA may be closely related with the development of Lyme neuroborreliosis.
莱姆神经Borreliosis 是一种由伯氏疏螺旋体（B. burgdorferi）引起的神经系统传染病。已证明伯氏疏螺旋体诱导的细胞因子与莱姆神经Borreliosis 有关。小胶质细胞被认为是中枢神经系统免疫反应中的关键参与者。在炎症反应中，它会被激活并产生细胞因子和趋化因子。体外细胞实验表明，伯氏疏螺旋体膜蛋白 A（BmpA）是伯氏疏螺旋体的主要免疫原，可诱导莱姆关节炎，并刺激人和鼠淋巴细胞产生炎症细胞因子。在我们的研究中，使用鼠小胶质细胞 BV2 细胞系作为细胞模型来探索重组 BmpA（rBmpA）的刺激作用；使用趋化因子芯片、ELISA 和 QPCR 技术来测量 rBmpA 刺激的小胶质细胞产生趋化因子。与阴性对照组相比，rBmpA 刺激后细胞上清液中 CXCL2、CCL22 和 CCL5 的浓度明显增加；随着 rBmpA 浓度的增加，这些趋化因子的浓度增加；10μg/mL 和 20μg/mL rBmpA 刺激后，鼠 BV2 细胞中趋化因子（CXCL2、CCL22 和 CCL5）的 mRNA 表达水平显著增加；rBmpA 刺激后 CXCL13 没有变化。我们的研究表明，rBmpA 在 BV2 细胞中上调了趋化因子，如 CXCL2、CCL22 和 CCL5。莱姆神经Borreliosis 中趋化因子的产生可能主要来自小胶质细胞，rBmpA 可能与莱姆神经Borreliosis 的发生发展密切相关。
