NF‑κB is a key modulator in the signaling pathway of Borrelia burgdorferi BmpA‑induced inflammatory chemokines in murine microglia BV2 cells.

NF‑κB is a key modulator in the signaling pathway of Borrelia burgdorferi BmpA‑induced inflammatory chemokines in murine microglia BV2 cells.
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DOI:
10.3892/mmr.2018.8526
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发表时间:
2018-04
影响因子:
3.4
通讯作者:
Bao F
Bao F
中科院分区:
医学4区
文献类型:
--
作者:
Zhao Z;Tao L;Liu A;Ma M;Li H;Zhao H;Yang J;Wang S;Jin Y;Shao X;Bao F

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莱姆病是由伯氏疏螺旋体引起的,是一种由壁虱传播的人畜共患病。莱姆病是莱姆病的主要表现,其发病机制尚不完全清楚。最近的研究表明,伯氏疏螺旋体脂蛋白引起的炎症效应与莱姆氏疏螺旋体病相似。碱性膜蛋白A是伯氏疏螺旋体膜上的主要脂蛋白之一。此外,核因子κ-B(NF-κB)调节与免疫和炎症相关的基因转录;然而,在未刺激的细胞中,NF-κB与NF-κB的抑制物(IκB-β)结合。因此,推测NF-κB可能与BMPA诱导的炎症和莱姆氏病的发生有关。因此,本研究的目的是探讨核因子-κB在rBmpA诱导的炎性趋化因子信号通路中的作用。本研究检测了重组BmPA(RBmpA)刺激小鼠小胶质细胞BV2后,NF-κB、I-κB-β和炎性趋化因子的表达水平。用rBmpA刺激后,用ELISA法测定C-X-C基序趋化因子2、C-C基序趋化因子5和CCL22等促炎细胞因子的浓度。逆转录-定量聚合酶链式反应和免疫印迹法检测NF-κB p65和IκB-β的表达水平。结果表明,rBmpA刺激后,这些趋化因子在细胞上清液中的浓度显著增加。NF-κB高表达,而I-κB-β表达显著降低。综上所述,这些结果表明,NF-κB在rBmpA诱导的BV2细胞炎性趋化因子的信号通路中起重要的刺激作用。
Lyme disease, caused by the bacterial spirochete Borrelia burgdorferi, is a tick-borne zoonosis. Lyme neuroborreliosis is a principal manifestation of Lyme disease and its pathogenesis remains incompletely understood. Recent studies have demonstrated that Borrelia burgdorferi lipoproteins caused similar inflammatory effects as exhibited in Lyme neuroborreliosis. Basic membrane protein A (BmpA) is one of the dominant lipoproteins in the Borrelia burgdorferi membrane. In addition, nuclear factor κ-B (NF-κB) modulates the regulation of gene transcription associated with immunity and inflammation; however, in unstimulated cells, NF-κB is combined with the inhibitor of NF-κB (IκB-β). Therefore, it was hypothesized that NF-κB may be associated with BmpA-induced inflammation and the occurrence of Lyme neuroborreliosis. Therefore, the aim of the present study was to investigate the role that NF-κB serves in the signaling pathway of rBmpA-induced inflammatory chemokines. The present study measured the expression levels of NF-κB, IκB-β and inflammatory chemokines following recombinant BmpA (rBmpA) stimulation of murine microglia BV2 cells. Following stimulation with rBmpA, concentrations of pro-inflammatory cytokines including C-X-C motif chemokine 2, C-C motif chemokine (CCL) 5 and CCL22 were determined by ELISA analysis. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to detect the expression levels of NF-κB p65 and IκB-β. The data demonstrated that concentrations of these chemokines in cell supernatants increased significantly following rBmpA stimulation. NF-κB was overexpressed, but IκB-β expression was significantly decreased. In conclusion, these results suggested that NF-κB serves an important stimulatory role in the signaling pathway of rBmpA-induced inflammatory chemokines in BV2 cells.
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