Τίτλος:
Impaired virus replication and decreased innate immune responses to viral infections in nasal epithelial cells from patients with allergic rhinitis
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
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. © 2016 British Society for Immunology
Συγγραφείς:
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.
Περιοδικό:
Clinical and Experimental Immunology
Εκδότης:
Wiley-Blackwell Publishing Ltd
Λέξεις-κλειδιά:
alpha interferon; antihistaminic agent; beta interferon; corticosteroid; interferon regulatory factor 3; interferon regulatory factor 7; messenger RNA; RANTES; toll like receptor 3; toll like receptor 7; toll like receptor 8; transcription factor 3; imidazole derivative; interferon; interferon regulatory factor 7; IRF7 protein, human; polyinosinic polycytidylic acid; RANTES; resiquimod; TLR3 protein, human; TLR7 protein, human; toll like receptor 3; toll like receptor 7, adult; allergic rhinitis; Article; cell proliferation; clinical article; controlled study; correlational study; epithelium cell; female; gene dosage; gene expression; human; Human parainfluenza virus 3; innate immunity; male; nasal epithelial cell; Parainfluenza virus infection; picornavirus infection; priority journal; protein expression; protein secretion; real time polymerase chain reaction; Rhinovirus; Rhinovirus serotype 1B; virus gene; virus replication; agonists; allergic rhinitis; cell culture; common cold; drug effects; epithelium cell; genetics; immunology; metabolism; middle aged; nose; pathology; physiology; Respirovirus infection; virology; young adult, Adult; Cells, Cultured; Chemokine CCL5; Common Cold; Epithelial Cells; Female; Humans; Imidazoles; Immunity, Innate; Interferon Regulatory Factor-7; Interferons; Male; Middle Aged; Nose; Parainfluenza Virus 3, Human; Poly I-C; Respirovirus Infections; Rhinitis, Allergic; Rhinovirus; Toll-Like Receptor 3; Toll-Like Receptor 7; Virus Replication; Young Adult
