ArticleExperimental biology and medicine (Maywood, N.J.)2022
Toll-like receptor 3 signaling induces interferon-induced transmembrane protein 1 in BEAS-2B cells.
Article in Experimental biology and medicine (Maywood, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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. Polyinosinic:polycytidylic acid (poly I:C) 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-β and ISG56 on IFITM1 upregulation. Poly I:C treatment significantly upregulated IFITM1 expression in BEAS-2B cells, and it was concentration- and time-dependent. Knockdown of IFN-β or ISG56 decreased poly I:C-induced IFITM1 expression levels. Recombinant IFN-β also increased expression levels of IFITM1. In BEAS-2B cells, IFITM1 expression is upregulated by poly I:C, at least partly, via the TLR3/IFN-β/ISG56 axis. Thus, IFITM1 may contribute to antiviral innate immunity in bronchial epithelium.
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