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Published on: January 21, 2018
Mast cells are permissive for rhinovirus replication: potential implications for asthma exacerbations
C Akoto1, D E Davies1,2, E J Swindle1,2
1Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, University Hospital Southampton, Southampton, UK.
Human rhinoviruses (HRVs) infect mast cells (MCs), driving asthma exacerbations. Exogenous interferon-beta (IFN-β) prevents HRV replication in MCs, suggesting a new therapeutic target for asthma.
Area of Science:
- Immunology
- Virology
- Respiratory Medicine
Background:
- Human rhinoviruses (HRVs) are a primary cause of asthma exacerbations.
- The bronchial epithelium is the main site of HRV infection.
- Mast cells (MCs) are increasingly implicated in asthma pathogenesis.
Purpose of the Study:
- To investigate if HRV infection of MCs elicits protective innate immune responses.
- To explore the role of MCs in HRV-induced asthma exacerbations.
Main Methods:
- Infection of MC lines (LAD2) and primary human cord blood-derived MCs (CBMCs) with HRV.
- Assessment of innate immune responses (IFN-β, IFN-λ, ISGs) via RT-qPCR and ELISA.
- Quantification of viral replication and infectious virion release.
Main Results:
- HRV infection induced IFN-β, IFN-λ, and ISG expression in MCs.
- MCs were permissive to HRV replication and release.
- Exogenous IFN-β, but not IFN-λ, protected MCs against HRV infection, while endogenous IFN signaling offered limited protection.
Conclusions:
- MCs support HRV replication and release.
- Exogenous IFN-β treatment can prevent HRV replication in MCs.
- MCs may represent a novel mechanism contributing to HRV-induced asthma exacerbations.
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