Expression of ISG60 is induced by TLR3 signaling in BEAS2B bronchial epithelial cells: Possible involvement in CXCL10 expression.
Mol Med Rep
; 30(3)2024 Sep.
Article
en En
| MEDLINE
| ID: mdl-38963029
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 noncancerous bronchial epithelial BEAS2B cells exposed to a Tolllike receptor 3 agonist. BEAS2B cells were treated with a synthetic TLR3 ligand, polyinosinicpolycytidylic acid (poly IC). The mRNA and protein expression levels of ISG60 were analyzed using reverse transcriptionquantitative PCR and western blotting, respectively. The levels of CXC motif chemokine ligand 10 (CXCL10) were examined using an enzymelinked immunosorbent assay, and the effects of knockdown of IFNß, ISG60 and ISG56 were examined using specific small interfering RNAs. Notably, ISG60 expression was increased in proportion to poly IC concentration, and recombinant human IFNß also induced ISG60 expression. By contrast, knockdown of IFNß 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.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Bronquios
/
Transducción de Señal
/
Poli I-C
/
Células Epiteliales
/
Receptor Toll-Like 3
/
Quimiocina CXCL10
Límite:
Humans
Idioma:
En
Revista:
Mol Med Rep
Año:
2024
Tipo del documento:
Article
País de afiliación:
Japón
Pais de publicación:
Grecia