Impaired virus replication and decreased innate immune responses to viral infections in nasal epithelial cells from patients with allergic rhinitis

• Published in: Clinical and experimental immunology Vol. 187; no. 1; pp. 100 - 112
• Main Authors: Głobińska, A., Pawełczyk, M., Piechota‐Polańczyk, A., Olszewska‐Ziąber, A., Moskwa, S., Mikołajczyk, A., Jabłońska, A., Zakrzewski, P. K., Brauncajs, M., Jarzębska, M., Taka, S., Papadopoulos, N. G., Kowalski, M. L.
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 01.01.2017; John Wiley and Sons Inc
• Subjects: Adult; allergic rhinitis; Allergies; Cells, Cultured; Chemokine CCL5 - genetics; Chemokine CCL5 - metabolism; Common Cold - immunology; Enterovirus; Epithelial Cells - drug effects; Epithelial Cells - immunology; Epithelial Cells - virology; Female; Humans; Imidazoles - pharmacology; Immunity, Innate; Infections; Interferon Regulatory Factor-7 - genetics; Interferon Regulatory Factor-7 - metabolism; interferons; Interferons - genetics; Interferons - metabolism; Male; Middle Aged; Nose - pathology; Original; parainfluenza type 3 virus; Parainfluenza Virus 3, Human - physiology; Paramyxoviridae; Picornaviridae; Poly I-C - pharmacology; primary nasal epithelial cells; Respirovirus Infections - immunology; Rhinitis, Allergic - immunology; Rhinitis, Allergic - virology; Rhinovirus - physiology; rhinovirus 1B; Toll-Like Receptor 3 - agonists; Toll-Like Receptor 7 - agonists; Viral infections; Virus Replication; Viruses; Young Adult; interferons; allergic rhinitis; rhinovirus 1B; primary nasal epithelial cells; parainfluenza type 3 virus
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/cei.12869

Summary The aim of this study was to assess the immune response to parainfluenza virus type 3 (PIV3), rhinovirus 1B (RV1B) and intracellular Toll‐like receptors (TLR) agonists in nasal epithelial cells (NECs) from patients with allergic rhinitis and healthy controls. NECs were obtained from eight patients with allergic rhinitis (AR) and 11 non‐atopic healthy controls (HC) by nasal scraping, grown to confluence and exposed to PIV3, RV1B infection or TLR‐3 and TLR‐7/8 agonists. Interferon (IFN)‐λ1, IFN‐α, IFN‐β and regulated on activation, normal T expressed and secreted (RANTES) release into the cell culture supernatants was assessed at 8, 24 and 48 h upon infection or 8 and 24 h after stimulation with poly(I:C) and R848. mRNA levels of IFNs, RANTES, interferon regulatory transcription factor (IRF)3, IRF7 and viral gene copy number were determined using real‐time polymerase chain reaction (RT‐PCR). PIV3 but not RV1B replication 48 h after infection was significantly lower (P < 0·01) in NECs from AR patients compared to HC. PIV3 infection induced significantly less IFN‐λ1 (both protein and mRNA) in NECs from AR compared to HC. IFN‐β mRNA expression and RANTES protein release and mRNA expression tended to be smaller in AR compared HC cells in response to both viruses. Stimulation with TLR‐3 agonist [poly (I:C)] induced similar IFN‐λ1 and RANTES generation in AR and HC subjects. Viral infections in NECs induced IRF7 expression, which correlated with IFN and RANTES expression. These data suggest that virus proliferation rates and the immune response profile are different in nasal epithelial cells from patients with allergic rhinitis compared to healthy individuals. The study demonstrated impaired immune response to viral infections in nasal epithelial cells (NECs) from allergic rhinitis patients. Significant differences in viral proliferation and innate response to parainfluenza type 3 (PIV3) and to a lesser extent to rhinovirus 1B (RV1B) in NECs from atopic donors as compared to healthy individuals have been shown.