Expression of ISG60 is induced by TLR3 signaling in BEAS‑2B bronchial epithelial cells: Possible involvement in CXCL10 expression.

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.