Abstract：
Viral infections in the respiratory tract are common, and, in recent years, severe acute respiratory syndrome coronavirus 2 outbreaks have highlighted the effect of viral infections on antiviral innate immune and inflammatory reactions. Specific treatments for numerous viral respiratory infections have not yet been established and they are mainly treated symptomatically. Therefore, understanding the details of the innate immune system underlying the airway epithelium is crucial for the development of new therapies. The present study aimed to investigate the function and expression of interferon (IFN)‑stimulated gene (ISG)60 in non‑cancerous bronchial epithelial BEAS‑2B cells exposed to a Toll‑like receptor 3 agonist. BEAS‑2B cells were treated with a synthetic TLR3 ligand, polyinosinic‑polycytidylic acid (poly IC). The mRNA and protein expression levels of ISG60 were analyzed using reverse transcription‑quantitative PCR and western blotting, respectively. The levels of C‑X‑C motif chemokine ligand 10 (CXCL10) were examined using an enzyme‑linked immunosorbent assay, and the effects of knockdown of IFN‑β, ISG60 and ISG56 were examined using specific small interfering RNAs. Notably, ISG60 expression was increased in proportion to poly IC concentration, and recombinant human IFN‑β also induced ISG60 expression. By contrast, knockdown of IFN‑β and ISG56 decreased ISG60 expression, and ISG60 knockdown reduced CXCL10 and ISG56 expression. These findings suggested that ISG60 is partly implicated in CXCL10 expression and that ISG60 may serve a role in the innate immune response of bronchial epithelial cells. The present study highlights ISG60 as a potential target for new therapeutic strategies against viral infections in the airway.
摘要：
呼吸道病毒感染很常见，and,近年来,严重急性呼吸道综合征冠状病毒2的爆发突显了病毒感染对抗病毒先天性免疫和炎症反应的影响.许多病毒性呼吸道感染的特异性治疗尚未建立，它们主要是对症治疗。因此,了解气道上皮固有免疫系统的细节对于开发新的治疗方法至关重要.本研究旨在研究暴露于Toll样受体3激动剂的非癌性支气管上皮BEAS-2B细胞中干扰素（IFN）刺激基因（ISG）60的功能和表达。BEAS‑2B细胞用合成TLR3配体处理，聚肌苷酸-聚胞苷酸（聚IC）。使用逆转录定量PCR和蛋白质印迹分析ISG60的mRNA和蛋白质表达水平，分别。使用酶联免疫吸附测定法检查C‑X‑C基序趋化因子配体10（CXCL10）的水平，以及IFN-β敲低的影响，使用特异性小干扰RNA检查ISG60和ISG56。值得注意的是,ISG60表达与polyIC浓度成比例增加，和重组人IFN-β也诱导ISG60表达。相比之下,IFN-β和ISG56的敲减降低了ISG60的表达，和ISG60敲低降低CXCL10和ISG56表达。这些发现表明ISG60部分参与CXCL10的表达,并且ISG60可能在支气管上皮细胞的先天免疫应答中起作用。本研究强调ISG60是针对气道病毒感染的新治疗策略的潜在靶标。
