Mouse models of rhinovirus-induced disease and exacerbation of allergic airway inflammation
Open accessAbstract
Rhinoviruses cause serious morbidity and mortality as the major etiological agents of asthma exacerbations and the common cold. A major obstacle to understanding disease pathogenesis and to the development of effective therapies has been the lack of a small-animal model for rhinovirus infection. Of the 100 known rhinovirus serotypes, 90% (the major group) use human intercellular adhesion molecule-1 (ICAM-1) as their cellular receptor and do not bind mouse ICAM-1; the remaining 10% (the minor group) use a member of the low-density lipoprotein receptor family and can bind the mouse counterpart. Here we describe three novel mouse models of rhinovirus infection: minor-group rhinovirus infection of BALB/c mice, major-group rhinovirus infection of transgenic BALB/c mice expressing a mouse-human ICAM-1 chimera and rhinovirus-induced exacerbation of allergic airway inflammation. These models have features similar to those observed in rhinovirus infection in humans, including augmentation of allergic airway inflammation, and will be useful in the development of future therapies for colds and asthma exacerbations.
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Murine models of combined rhinovirus infection and exposure to airway allergens give enhanced Th2 responses compared to those to virus or allergen challenge alone.
“murine models of combined rhinovirus infection and exposure to airway allergens give enhanced Th2 responses compared to those to virus or allergen challenge alone (14, 193).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [14]
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- Authors
- Bartlett, N. W., Walton, R. P., Edwards, M. R., Aniscenko, J., Caramori, G., Zhu, J., Glanville, N., Choy, K. J., Jourdan, P., Burnet, J., Tuthill, T. J., Pedrick, M. S., Hurle, M. J., Plumpton, C., Sharp, N. A., Bussell, J. N., Swallow, D. M., Schwarze, J., Guy, B., Almond, J. W., Jeffery, P. K., Lloyd, C. M., Papi, A., Killington, R. A., Rowlands, D. J., Blair, E. D., Clarke, N. J., & Johnston, S. L.
- Affiliations
- Asthma UK (GB)
- National Institutes of Health (US)
- University of Ferrara (IT)
- Imperial College London (GB)
- University of Leeds (GB)
- GlaxoSmithKline (United Kingdom) (GB)
- University College London (GB)
- Sanofi (France) (FR)
- Corresponding author
- Johnston, Sebastian L
- ORCID
- Venue
- Nature Medicine
- Published
- 2008-02
- Volume
- 14
- Issue
- 2
- Pages
- 199-204
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3384678
- OpenAlex
- W2065220920
- Cited by
- 375
- References
- 34
- Citations by year
- 2026: 9 · 2025: 16 · 2024: 7 · 2023: 7 · 2022: 17 · 2021: 17 · 2020: 16 · 2019: 15 · 2018: 20 · 2017: 27 · 2016: 18 · 2015: 20 · 2014: 29 · 2013: 38 · 2012: 22
- FWCI
- 24.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion)
- Funders
- Wellcome Trust (087618, 057704)
- Topics
- Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Keywords
- rhinovirus infection, mouse model, allergic airway inflammation, asthma exacerbations, common cold, ICAM-1, transgenic mice, LDL receptor, viral receptor specificity
- MeSH terms
- Animals, Antibody Formation, Chemotactic Factors, Dendritic Cells, Disease Models, Animal, Humans, Hypersensitivity, Immunity, Innate, Inflammation, Mice, Transgenic, Mucus, Neutrophils, Picornaviridae Infections, Respiratory System, Rhinovirus, Ultraviolet Rays, Virus Replication, Bronchial Hyperreactivity, Th1 Cells, Th2 Cells, Intercellular Adhesion Molecule-1, Inflammation Mediators, Chemokines, Virus Inactivation, Mice
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