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)
|