Impaired virus replication and decreased innate immune responses to viral infections in nasal epithelial cells from patients with allergic rhinitis.
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.
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Głobińska
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Pawełczyk
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Piechota-Polańczyk
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Olszewska-Ziąber
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.|Microbiology and Laboratory Medical Immunology Department, Medical University of Łódź, Łódź, Poland.
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Moskwa
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Mikołajczyk
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Jabłońska
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Zakrzewski
Microbiology and Laboratory Medical Immunology Department, Medical University of Łódź, Łódź, Poland.
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Brauncajs
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Jarzębska
Allergy Department, Second Paediatric Clinic, University of Athens, Athens, Greece.
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Taka
Allergy Department, Second Paediatric Clinic, University of Athens, Athens, Greece.
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Papadopoulos
Department of Immunology, Rheumatology and Allergy, Medical University of Łódź, Łódź, Poland.|Healthy Ageing Research Center, Medical University of Łódź, Łódź, Poland.
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Kowalski
D000328:Adult; D002478:Cells, Cultured; D018946:Chemokine CCL5 / Q000235:genetics / Q000378:metabolism; D003139:Common Cold / Q000276:immunology*; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology* / Q000821:virology; D005260:Female; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007113:Immunity, Innate; D050839:Interferon Regulatory Factor-7 / Q000235:genetics / Q000378:metabolism; D007372:Interferons / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009666:Nose / Q000473:pathology; D010224:Parainfluenza Virus 3, Human / Q000502:physiology*; D011070:Poly I-C / Q000494:pharmacology; D010253:Respirovirus Infections / Q000276:immunology*; D065631:Rhinitis, Allergic / Q000276:immunology* / Q000821:virology; D012229:Rhinovirus / Q000502:physiology*; D051196:Toll-Like Receptor 3 / Q000819:agonists; D051199:Toll-Like Receptor 7 / Q000819:agonists; D014779:Virus Replication; D055815:Young Adult
D018946:Chemokine CCL5; C494234:IRF7 protein, human; D007093:Imidazoles; D050839:Interferon Regulatory Factor-7; C495344:TLR3 protein, human; C495348:TLR7 protein, human; D051196:Toll-Like Receptor 3; D051199:Toll-Like Receptor 7; D007372:Interferons; D011070:Poly I-C; C402365:resiquimod
allergic rhinitis; interferons; parainfluenza type 3 virus; primary nasal epithelial cells; rhinovirus 1B
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