A Comprehensive Evaluation of Nasal and Bronchial Cytokines and Chemokines Following Experimental Rhinovirus Infection in Allergic Asthma: Increased Interferons (IFN-γ and IFN-λ) and Type 2 Inflammation (IL-5 and IL-13)
Trevor T. Hansel,
Tanushree Tunstall,
Maria-Belen Trujillo-Torralbo,
Betty Shamji,
Ajerico del-Rosario,
Jaideep Dhariwal,
Paul D.W. Kirk,
Michael P.H. Stumpf,
Jens Koopmann,
Aurica Telcian,
Julia Aniscenko,
Leila Gogsadze,
Eteri Bakhsoliani,
Luminita Stanciu,
Nathan Bartlett,
Michael Edwards,
Ross Walton,
Patrick Mallia,
Toby M. Hunt,
Trevor L. Hunt,
Duncan G. Hunt,
John Westwick,
Matthew Edwards,
Onn Min Kon,
David J. Jackson,
Sebastian L. Johnston
Affiliations
Trevor T. Hansel
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Tanushree Tunstall
Imperial College Healthcare NHS Trust, UK
Maria-Belen Trujillo-Torralbo
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Betty Shamji
Novartis Institute for Biomedical Research, Horsham, UK
Ajerico del-Rosario
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Jaideep Dhariwal
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Paul D.W. Kirk
MRC Biostatistics Unit, Cambridge Institute of Public Health, Cambridge, UK
Michael P.H. Stumpf
Dept. of Theoretical Systems Biology at IC, UK
Jens Koopmann
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Aurica Telcian
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Julia Aniscenko
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Leila Gogsadze
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Eteri Bakhsoliani
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Luminita Stanciu
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Nathan Bartlett
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Michael Edwards
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Ross Walton
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Patrick Mallia
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Toby M. Hunt
Hunt Developments (UK) Ltd, Midhurst, West Sussex, UK
Trevor L. Hunt
Hunt Developments (UK) Ltd, Midhurst, West Sussex, UK
Duncan G. Hunt
Hunt Developments (UK) Ltd, Midhurst, West Sussex, UK
John Westwick
Novartis Institute for Biomedical Research, Horsham, UK
Matthew Edwards
Novartis Institute for Biomedical Research, Horsham, UK
Onn Min Kon
Imperial College Healthcare NHS Trust, UK
David J. Jackson
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Sebastian L. Johnston
Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College (IC), London, UK
Background: Rhinovirus infection is a major cause of asthma exacerbations. Objectives: We studied nasal and bronchial mucosal inflammatory responses during experimental rhinovirus-induced asthma exacerbations. Methods: We used nasosorption on days 0, 2–5 and 7 and bronchosorption at baseline and day 4 to sample mucosal lining fluid to investigate airway mucosal responses to rhinovirus infection in patients with allergic asthma (n = 28) and healthy non-atopic controls (n = 11), by using a synthetic absorptive matrix and measuring levels of 34 cytokines and chemokines using a sensitive multiplex assay. Results: Following rhinovirus infection asthmatics developed more upper and lower respiratory symptoms and lower peak expiratory flows compared to controls (all P < 0.05). Asthmatics also developed higher nasal lining fluid levels of an anti-viral pathway (including IFN-γ, IFN-λ/IL-29, CXCL11/ITAC, CXCL10/IP10 and IL-15) and a type 2 inflammatory pathway (IL-4, IL-5, IL-13, CCL17/TARC, CCL11/eotaxin, CCL26/eotaxin-3) (area under curve day 0–7, all P < 0.05). Nasal IL-5 and IL-13 were higher in asthmatics at day 0 (P < 0.01) and levels increased by days 3 and 4 (P < 0.01). A hierarchical correlation matrix of 24 nasal lining fluid cytokine and chemokine levels over 7 days demonstrated expression of distinct interferon-related and type 2 pathways in asthmatics. In asthmatics IFN-γ, CXCL10/IP10, CXCL11/ITAC, IL-15 and IL-5 increased in bronchial lining fluid following viral infection (all P < 0.05). Conclusions: Precision sampling of mucosal lining fluid identifies robust interferon and type 2 responses in the upper and lower airways of asthmatics during an asthma exacerbation. Nasosorption and bronchosorption have potential to define asthma endotypes in stable disease and at exacerbation.