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瘤坏死因子和中白素-1β 抑制NRP2表达并促进SARS-CoV-2的扩散

Michinori Ishitoku¹, Sho Mokuda^1,2, Kei Araki¹

¹Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima 734-8551, Japan.

|July 29, 2023

概括

支持炎症的细胞因子,如瘤坏死因子α (TNFα) 和互白素-1β (IL-1β) 增加神经皮林-2 (NRP2) 的表达. 这种上调增强了严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 的扩散和人类细胞中的尖端蛋白结合.

科学领域:

病毒学病毒学
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 使用ACE2和神经平素-1 (NRP1) 进入细胞.
在COVID-19病变发生过程中,NRP1的异形Neuropilin-2 (NRP2) 的作用在很大程度上尚未被探索.
在严重的COVID-19和病毒复制中增加的促炎细胞因子之间的联系是未知的.

研究的目的:

研究促炎性细胞因子在调节神经皮林 (NRP) 表达中的作用.
确定细胞因子诱导的NRP表达对SARS-CoV-2感染和扩散的影响.

主要方法:

使用了下一代测序 (RNA-seq),免疫组织化学,定量实时PCR和西式涂抹.
在炎症和非炎症条件下,检查了NRP表达在纤维细胞样突细胞,MH7A,MRC5细胞系和突组织中.
进行了SARS-CoV-2感染实验,以评估病毒扩散和Spike蛋白结合.

主要成果:

在炎症组织中,神经皮林-2 (NRP2) 表达显著上调.
与瘤坏死因子α (TNFα) 和互白素-1β (IL-1β) 联合刺激增加了人类纤维细胞细胞系中的NRP2表达.
TNFα和IL-1β促进了SARS-CoV-2的扩散和Spike蛋白的结合,与NRP2表达水平相关.

结论:

促炎性细胞因子,特别是TNFα和IL-1β,驱动宿主细胞中的NRP2上调.
在促进SARS-CoV-2的扩散和感染方面,NRP2起着至关重要的作用.
向细胞因子诱导的NRP2表达可能提供针对COVID-19的治疗策略.

关键词:

神经活素-1 (NRP1) 是一种神经活素.神经平素-2 (NRP2) 是一种神经平素.冠状病毒疾病2019 (COVID-19) 是一种新型冠状病毒疾病.严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2)瘤死亡因子α (TNFα)

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