在简单疹病毒潜伏建立期间,TNF-α对电压通道的调节
Qiaojuan Zhang1, Shao-Chung Hsia1, Miguel Martin-Caraballo2
1Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland Eastern Shore, Princess Anne, MD, 21853, USA.
简单疹病毒1型 (HSV-1) 感染会降低感官神经元中的通道功能. 瘤亡因子-α (TNF-α) 抵消了这种效应,在HSV-1潜伏期间保持疼痛信号传输.
科学领域:
- 神经科学是一个神经科学.
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
背景情况:
- 简单疹病毒1型 (HSV-1) 感染改变了感觉神经元中的电压接 (Na+) 通道表达,可能破坏疼痛信号传递.
- HSV-1感染还会触发诸如TNF-α和IL-6之类的促炎细胞因子.
研究的目的:
- 调查TNF-α是否调节HSV-1潜伏期在感觉类神经元中建立的Na+通道表达.
- 了解TNF-α在维持HSV-1感染期间疼痛信息传输中的作用.
主要方法:
- 在使用阿西克洛维尔 (ACV) 的ND7/23细胞中确立了HSV-1潜伏期.
- 整个细胞记录评估了电压关闭的Na+通道的功能表达.
- 用TNF-α或IL-6治疗细胞,并使用p38信号通路抑制剂 (SB203580,SB202190).
主要成果:
- 在潜伏期内,HSV-1感染显著降低了电流.
- 暴露于TNF-α可以逆转HSV-1的作用,增加的电流密度,而不会改变道特性.
- IL-6没有恢复Na+电流. 刺激TNF-α激活了p38信号,这对于它对电流的影响至关重要.
结论:
- 在HSV-1潜伏期间,TNF-α信号升级调节传感神经元中电压通的Na+通道表达.
- 这种TNF-α的上调有助于维持疼痛信号传输,尽管HSV-1感染.
- p38信号通路调解TNF-α对Na+通道的调节作用.
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