Synthetic double-stranded RNA induces interleukin-32 in bronchial epithelial cells

Abstract

The expression of IL-32 is induced by dsRNA via the TAK1-NF-κB signaling pathway in bronchial epithelial cells. IL-32 is involved in the pathogenesis of airway inflammation, and may be a novel therapeutic target for airway inflammatory diseases.

The IL-37–Mex3B–Toll-like receptor 3 axis in epithelial cells in patients with eosinophilic chronic rhinosinusitis with nasal polyps

“…25 BEAS-2B cells were transfected with small interfering RNA targeting Mex3B (siMex3B; Invitrogen, Thermo Fisher Scientific, Waltham, Mass) or recombinant lentiviral vectors carrying the human Mex3B gene (Ltv-Mex3B; GeneChem, Shanghai, China), as previously described. 29,30 After transfection, BEAS-2B cells were further stimulated with polyinosinic-polycytidylic acid (poly[I:C]; Tocris Bioscience, Bristol, United Kingdom) and rhIL-37b (Val46-Asp218; R&D Systems, Minneapolis, Minn). More information is provided in the Methods section in this article's Online Repository.…”

“…25 In some experiments respiratory sinonasal mucosa was dissected under a microscope, and total RNA was extracted for quantitative RT-PCR assay. 25,29 More information is provided in the Methods section in this article's Online Repository.…”

Interferon‐γ‐induced insufficient autophagy contributes to p62‐dependent apoptosis of epithelial cells in chronic rhinosinusitis with nasal polyps

“…Small interfering RNA (siRNA) transfection was performed as previously described. 29 siRNAs were synthesized by Invitrogen Thermo Fisher Scientific Company (Waltham, MA, USA). Polyp NECs were transfected with nonspecific control siRNA (siNS) or siRNA targeting p62 (sip62).…”

Interleukin 32: a novel player in the control of infectious diseases

“…These include the TLR4 agonist LPS, TLR2 agonists zymosan and triacylated lipopeptide, and muramyl dipeptide signaling via the NOD2 receptor. Similarly, the signaling effects of factors associated with viral infection on IL-32 production are reported to occur via TLR3 (in the case of dsRNA), as well as propagated by influenza virus protein in epithelial cells [6,22,23]. During influenza virus infection, NF-kB, CREB, and COX-2 expression/PGE 2 pathways are activated to promote IL-32 production in epithelial cells [19,24].…”