A key protein from Borrelia burgdorferi could stimulate cytokines in human microglial cells and inhibitory effects of Cucurbitacin IIa

IF 2 Q3 NEUROSCIENCES
Xin Xu , Shiyuan Wen , Yu Zhang , Wenjing Cao , Peng Yue , Jing Kong , Meixiao Liu , Yuxin Fan , Jingjing Chen , Zhenhua Ji , Yan Dong , Guozhong Zhou , Bingxue Li , Aihua Liu , Fukai Bao
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引用次数: 0

Abstract

Lyme neuroborreliosis (LNB) is an infectious disease of the nervous system caused by Borrelia burgdorferi (Bb) infection. However, its pathogenesis is not fully understood. We used recombinant BmpA (rBmpA) to stimulate human microglia cell HMC3, then collected the culture supernatant and extracted total RNA from cells, and used the supernatant for cytokine chip, then ELISA and qPCR technology were used to validate the results from cytokine chip. After rBmpA stimulation of microglia, 24 inflammation-related cytokines showed elevated expression. Among them, six cytokines (IL-6, IL-8, CCL2, CCL5, CXCL1, and CXCL10) increased significantly in mRNA transcription, three cytokines (IL-6, IL-8, and CXCL10) concentrations in the cell supernatant increased significantly after the rBmpA stimulation, and CuIIa could inhibit expression of these cytokines. The BmpA can stimulate human microglia to produce large amounts of cytokines, leading to the occurrence of inflammation, which may be closely related to the development of LNB. CuIIa can inhibit BmpA-induced cytokine production in microglia, which may have potential therapeutic effects on LNB.

伯氏疏螺旋体的一个关键蛋白可以刺激人小胶质细胞的细胞因子并抑制葫芦素IIa
莱姆病是一种由伯氏疏螺旋体(Bb)感染引起的神经系统感染性疾病。然而,其发病机制尚不完全清楚。用重组BmpA (rBmpA)刺激人小胶质细胞HMC3,收集培养上清,提取细胞总RNA,将上清用于细胞因子芯片,采用ELISA和qPCR技术验证细胞因子芯片结果。rBmpA刺激小胶质细胞后,24种炎症相关细胞因子表达升高。其中,6种细胞因子(IL-6、IL-8、CCL2、CCL5、CXCL1、CXCL10) mRNA转录显著升高,3种细胞因子(IL-6、IL-8、CXCL10)在rBmpA刺激后细胞上清浓度显著升高,CuIIa可抑制这些细胞因子的表达。BmpA可刺激人小胶质细胞产生大量细胞因子,导致炎症的发生,这可能与LNB的发生密切相关。CuIIa可以抑制bmpa诱导的小胶质细胞产生细胞因子,可能对LNB有潜在的治疗作用。
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来源期刊
IBRO Neuroscience Reports
IBRO Neuroscience Reports Neuroscience-Neuroscience (all)
CiteScore
2.80
自引率
0.00%
发文量
99
审稿时长
14 weeks
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