Innate Immune Response to Viral Infections in Primary Bronchial Epithelial Cells is Modified by the Atopic Status of Asthmatic Patients

Title: Innate Immune Response to Viral Infections in Primary Bronchial Epithelial Cells is Modified by the Atopic Status of Asthmatic Patients
Authors: Moskwa, S
Piotrowski, W
Marczak, J
Pawelczyk, M
Lewandowska-Polak, A
Jarzebska, M
Brauncajs, M
Globinska, A
Gorski, P
Papadopoulos, NG
Edwards, MR
Johnston, SL
Kowalski, ML
Item Type: Journal Article
Abstract: Purpose In order to gain an insight into determinants of reported variability in immune responses to respiratory viruses in human bronchial epithelial cells (HBECs) from asthmatics, the responses of HBEC to viral infections were evaluated in HBECs from phenotypically heterogeneous groups of asthmatics and in healthy controls. Methods HBECs were obtained during bronchoscopy from 10 patients with asthma (6 atopic and 4 non-atopic) and from healthy controls (n=9) and grown as undifferentiated cultures. HBECs were infected with parainfluenza virus (PIV)-3 (MOI 0.1) and rhinovirus (RV)-1B (MOI 0.1), or treated with medium alone. The cell supernatants were harvested at 8, 24, and 48 hours. IFN-α, CXCL10 (IP-10), and RANTES (CCL5) were analyzed by using Cytometric Bead Array (CBA), and interferon (IFN)-β and IFN-λ1 by ELISA. Gene expression of IFNs, chemokines, and IFN-regulatory factors (IRF-3 and IRF-7) was determined by using quantitative PCR. Results PIV3 and RV1B infections increased IFN-λ1 mRNA expression in HBECs from asthmatics and healthy controls to a similar extent, and virus-induced IFN-λ1 expression correlated positively with IRF-7 expression. Following PIV3 infection, IP-10 protein release and mRNA expression were significantly higher in asthmatics compared to healthy controls (median 36.03-fold). No differences in the release or expression of RANTES, IFN-λ1 protein and mRNA, or IFN-α and IFN-β mRNA between asthmatics and healthy controls were observed. However, when asthmatics were divided according to their atopic status, HBECs from atopic asthmatics (n=6) generated significantly more IFN-λ1 protein and demonstrated higher IFN-α, IFN-β, and IRF-7 mRNA expressions in response to PIV3 compared to non-atopic asthmatics (n=4) and healthy controls (n=9). In response to RV1B infection, IFN-β mRNA expression was lower (12.39-fold at 24 hours and 19.37-fold at 48 hours) in non-atopic asthmatics compared to atopic asthmatics. Conclusions The immune response of HBECs to virus infections may not be deficient in asthmatics, but seems to be modified by atopic status.
Issue Date: 1-Mar-2018
Date of Acceptance: 24-Sep-2017
URI: http://hdl.handle.net/10044/1/60328
DOI: https://dx.doi.org/10.4168/aair.2018.10.2.144
ISSN: 2092-7355
Publisher: KOREAN ACAD ASTHMA ALLERGY & CLINICAL IMMUNOLOGY
Start Page: 144
End Page: 154
Journal / Book Title: ALLERGY ASTHMA & IMMUNOLOGY RESEARCH
Volume: 10
Issue: 2
Copyright Statement: © 2018 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Sponsor/Funder: Commission of the European Communities
Medical Research Council (MRC)
Medical Research Council (MRC)
Funder's Grant Number: 260895
G1000758
G1000758
Keywords: Science & Technology
Life Sciences & Biomedicine
Allergy
Immunology
Asthma
bronchial epithelial cells
interferon
parainfluenza virus
rhinovirus
RHINOVIRUS INFECTION
RESPIRATORY VIRUSES
INTERFERON RESPONSE
POSITIVE FEEDBACK
INTRINSIC ASTHMA
IFN-BETA
IN-VIVO
EXACERBATIONS
CHILDREN
GENES
Publication Status: Published
Online Publication Date: 2018-01-09
Appears in Collections:National Heart and Lung Institute
Faculty of Medicine



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Creative Commons