Toll-like receptor 3 signaling induces interferon-induced transmembrane protein 1 in BEAS-2B cells.
Exp Biol Med (Maywood)
; 247(21): 1917-1922, 2022 11.
Article
en En
| MEDLINE
| ID: mdl-36112878
ABSTRACT
The human bronchial epithelium plays a crucial role in mediating antiviral immune reactions. When double-stranded RNA (dsRNA) binds to the receptor named Toll-like receptor (TLR) 3, activation of antiviral innate immune reactions is initiated by producing interferon (IFN) type I. Then, type I IFN promotes the transcription of IFN-stimulated genes (ISGs). Proteins encoded by ISGs reveal antiviral effects. The IFN-induced transmembrane protein 1 (IFITM1) is an ISG family member that inhibits viral infection by preventing the entry of viruses with a cell membrane. However, IFITM1 expression in human bronchial epithelium remains largely undetermined. Here, we investigated whether IFITM1 is expressed in cultured BEAS-2B bronchial epithelial cells. Polyinosinicpolycytidylic acid (poly IC) was used for treatment of BEAS-2B as a TLR3 ligand. IFITM1 expression levels were measured using reverse transcription-quantitative PCR and Western blotting. Using RNA interference, we determined the significance of IFN-ß and ISG56 on IFITM1 upregulation. Poly IC treatment significantly upregulated IFITM1 expression in BEAS-2B cells, and it was concentration- and time-dependent. Knockdown of IFN-ß or ISG56 decreased poly IC-induced IFITM1 expression levels. Recombinant IFN-ß also increased expression levels of IFITM1. In BEAS-2B cells, IFITM1 expression is upregulated by poly IC, at least partly, via the TLR3/IFN-ß/ISG56 axis. Thus, IFITM1 may contribute to antiviral innate immunity in bronchial epithelium.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Virosis
/
Antígenos de Diferenciación
/
Interferones
/
Receptor Toll-Like 3
Límite:
Humans
Idioma:
En
Revista:
Exp Biol Med (Maywood)
Asunto de la revista:
BIOLOGIA
/
FISIOLOGIA
/
MEDICINA
Año:
2022
Tipo del documento:
Article
País de afiliación:
Japón