STAT1 participates in the induction of substance P expression in airway epithelial cells by respiratory syncytial virus.

IF 1.5 4区医学 Q3 RESPIRATORY SYSTEM

Experimental Lung Research Pub Date : 2021-02-01 Epub Date: 2020-11-26 DOI:10.1080/01902148.2020.1850922

Yu-Long Luo, Sheng Wang, Zhi-Xin Fang, Yi-Chu Nie, Li-Ting Zhang, Chu-Qin Huang, Li Long, Ke-Fang Lai

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引用次数: 1

Abstract

Purpose: The regulation effect and mechanism of respiratory syncytial virus (RSV) infection on the expression of tachykinin substance P (SP) in airway epithelial cells was investigated.

Methods: The regulation of SP expression by RSV was investigated in the BEAS-2B airway epithelial cell line. RT-qPCR, immunofluorescence, and ELISA assay were used to examine the expression of the SP encoding gene TAC1, the intracellular SP protein expression, and the extracellular SP secretion.

Results: The mRNA expression of TAC1 and the intracellular SP protein level in BEAS-2B cells were significantly enhanced by RSV infection with multiplicity of infection (MOI) values of both 1 and 0.1 at 48 hours post infection. Heat-inactivated and UV-inactivated RSV, but not live RSV, significantly induced SP secretion in both control BEAS-2B cells and CX3CR1 receptor knockout cells without affecting the TAC1 gene expression or cell viability. RSV G protein (2-10 μg/ml) and fractalkine (10-50 ng/ml), both CX3CR1 receptor ligands, did not affect SP secretion in BEAS-2B cells. Inhibition of STAT1 phosphorylation by fludarabine (1 μM) markedly reduced the RSV-induced TAC1 gene expression and antagonized the inhibition of RSV replication by interferon-α in BEAS-2B cells.

Conclusions: STAT1 participates in RSV infection-induced SP expression in airway epithelial cells.

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STAT1参与呼吸道合胞病毒诱导气道上皮细胞P物质表达。

目的:探讨呼吸道合胞病毒(RSV)感染对气道上皮细胞速激肽物质P (SP)表达的调控作用及其机制。方法:研究RSV对BEAS-2B气道上皮细胞株SP表达的调控作用。采用RT-qPCR、免疫荧光和ELISA法检测SP编码基因TAC1的表达、胞内SP蛋白表达和胞外SP分泌情况。结果:感染RSV后48 h, BEAS-2B细胞TAC1 mRNA表达和胞内SP蛋白水平均显著升高，感染多重性(multiplicity of infection, MOI)分别为1和0.1。热灭活和紫外线灭活RSV，而非活RSV，在对照BEAS-2B细胞和CX3CR1受体敲除细胞中均显著诱导SP分泌，而不影响TAC1基因表达和细胞活力。CX3CR1受体配体RSV G蛋白(2 ~ 10 μg/ml)和fractalkine (10 ~ 50 ng/ml)对BEAS-2B细胞SP分泌均无影响。氟达拉滨(1 μM)抑制STAT1磷酸化可显著降低RSV诱导的TAC1基因表达，拮抗干扰素-α对BEAS-2B细胞RSV复制的抑制作用。结论:STAT1参与RSV感染诱导的气道上皮细胞SP的表达。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Experimental Lung Research 医学-呼吸系统

CiteScore

3.80

自引率

0.00%

发文量

审稿时长

2 months

期刊介绍： Experimental Lung Research publishes original articles in all fields of respiratory tract anatomy, biology, developmental biology, toxicology, and pathology. Emphasis is placed on investigations concerned with molecular, biochemical, and cellular mechanisms of normal function, pathogenesis, and responses to injury. The journal publishes reports on important methodological advances on new experimental modes. Also published are invited reviews on important and timely research advances, as well as proceedings of specialized symposia. Authors can choose to publish gold open access in this journal.