Allergy Asthma Immunol Res.  2018 Mar;10(2):144-154. 10.4168/aair.2018.10.2.144.

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

Affiliations
  • 1Department of Immunology, Rheumatology and Allergy; Healthy Ageing Research Centre, Medical University of Lodz, Lodz, Poland. marek.kowalski@csk.umed.lodz.pl
  • 2Department of Pneumonology and Allergy, Medical University of Lodz, Lodz, Poland.
  • 3Department of Microbiology and Laboratory Medical Immunology, Medical University of Lodz, Lodz, Poland.
  • 4Department of Rheumatology, Medical University of Lodz, Lodz, Poland.
  • 5Allergy Research Centre, 2nd Pediatric Clinic, National Kapodistrian, University of Athens, Athens, Greece.
  • 6National Heart and Lung Institute, Imperial College London, London, UK; Asthma UK Centre in Allergic Mechanisms of Asthma.

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.

Keyword

Asthma; bronchial epithelial cells; interferon; parainfluenza virus; rhinovirus

MeSH Terms

Asthma
Bronchi*
Bronchoscopy
Chemokine CCL5
Chemokines
Enzyme-Linked Immunosorbent Assay
Epithelial Cells*
Gene Expression
Humans
Immunity, Innate*
Interferons
Paramyxoviridae Infections
Polymerase Chain Reaction
Rhinovirus
RNA, Messenger
Chemokine CCL5
Chemokines
Interferons
RNA, Messenger
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