Evidence from the lab linking allergy to increased risk of epithelial cells viral infection Evidence from the lab linking allergy to increased risk of epithelial cells viral infection Evidence from the lab linking allergy to increased risk of epithelial cells viral infection Evidence from the lab linking allergy to increased risk of epithelial cells viral infection Evidence from the lab linking allergy to increased risk of epithelial cells viral infection Evidence from the lab linking allergy to increased risk of epithelial cells viral infection
Author Year (ref)
No. of cases
Experimental models
Methods
Relevant results
Association (Level of evidence)
Waltl et al. 2018 (12)
N=20
Cultured human cells from inferior nasal turbinate.
Impedance-based measurement of respiratory epithelial barrier function after the exposure to different concentrations of House dust mites (HDM) extract.
Dose dependent decrease of barrier function, alteration of morphology and thickness of the epithelium, decrease of ciliary beat frequency and tight junction expression, facilitating pathogen permeability.
Yes (Level V)
Steelant et al. 2016 (13)
N=25. 9 pz and 16 controls
Cultures of primary nasal epithelial cells of patients with HDM-induced allergic rhinitis (AR) and controls.
Measurement of transepithelial resistance and passage of fluorescein isothiocyanate-dextran 4 (FD4), quantitative PCR of tight junction expression and effects of IL-4, IFN-γ, and fluticasone propionate (FP).
AR have increased FD4 permeability and reduced occludin and zonula occludens-1 expression; in vitro IL-4 decreased transepithelial resistance and increased FD4 permeability, whereas IFN-γ had no effect. FP prevented IL-4-induced barrier dysfunction.
Yes (Level V)
Steelant et al. 2018 (14)
N= 9 allergic rhinitis; 6 idiopathic rhinitis; 10 controls.
Cultures of primary nasal epithelial cells from healthy control exposed to nasal secretions of allergic vs non-allergic patients.
Measurement of transepithelial electrical resistance, paracellular flux of fluorescein isothiocyanate-dextran 4 and mRNA expression of tight junctions.
Histamine and nasal secretions from AR, but not from idiopathic rhinitis patients, rapidly decrease in trans-tissue resistance. Pre-treatment with histamine receptor-1 antagonist, azelastine, prevented the early effect of nasal secretions of AR patients on epithelial integrity.
Yes (Level V)
Głobińska 2017 (18)
N=19 (8 AR and 11 healthy controls).
Cultured nasal epithelial cells (NECs) exposed to parainfluenza virus type 3 (PIV3), rhinovirus 1B (RV1B) and intracellular TLR agonists.
Interferon (IFN)-k1, IFN-a, IFN-b released into the cell culture supernatants was assessed at 8, 24 and 48 h upon infection; mRNA levels of IFNs, RANTES, were determined using real-time polymerase chain reaction (RT-PCR).
PIV3 infection induced significantly less IFN-k1 (both protein and mRNA) in NECs from AR compared to healthy controls. IFN-b mRNA expression and RANTES protein release tended to be smaller in AR compared controls cells in response to both viruses.
Yes (Level V)
Fenoglio et al. 2008 (19)
N=41 AR patients
Peripheral blood mononuclear cells (PBMC) producing IFN-in vitro.
IFN-γ-specific producing cells were stimulated with Phytohaemagglutinin (PHA), causal pollen, and House Dust Mite (HDM). IFN-γ production was assessed by cytokine ELISPOT.
IFN-γ production of PBMC stimulated by specific pollen was significantly lower than IFN-γ production of PBMC stimulated by HDM. IFN-γ production of PBMC stimulated by specific pollen was significantly lower than IFN-γ production of PBMC stimulated by PHA.
Yes (Level V)
Teach et al. 2015 (20)
N=478 children (10.2±2.93 yr).
Peripheral blood mononuclear cell cultures incubated ex-vivo with rhinovirus.
Measuring INF-α in supernatants of PBMCs cultures obtained from a subset of subjects (n = 87) incubated ex-vivo with rhinovirusin patients treated or not with Omalizumab.
The group treated with anti-IgE had improved INF-α production after virus infection suggesting restoring of the impaired interferon response and increasing antiviral immunity and suggesting that anti-IgE may prevent upper and lower respiratory infections and asthma exacerbations
Yes (Level V)