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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.
Background:
Human rhinoviruses (HRVs) are a major trigger of asthma exacerbations, with the bronchial epithelium being the major site of HRV infection and replication. Mast cells (MCs) play a key role in asthma where their numbers are increased in the bronchial epithelium with increasing disease severity.
Objective:
In view of the emerging role of MCs in innate immunity and increased localization to the asthmatic bronchial epithelium, we investigated whether HRV infection of MCs generated innate immune responses which were protective against infection.
Methods:
The LAD2 MC line or primary human cord blood-derived MCs (CBMCs) were infected with HRV or UV-irradiated HRV at increasing multiplicities of infection (MOI) without or with IFN-β or IFN-λ. After 24 h, innate immune responses were assessed by RT-qPCR and IFN protein release by ELISA. Viral replication was determined by RT-qPCR and virion release by TCID50 assay.
Results:
HRV infection of LAD2 MCs induced expression of IFN-β, IFN-λ and IFN-stimulated genes. However, LAD2 MCs were permissive for HRV replication and release of infectious HRV particles. Similar findings were observed with CBMCs. Neutralization of the type I IFN receptor had minimal effects on viral shedding, suggesting that endogenous type I IFN signalling offered limited protection against HRV. However, augmentation of these responses by exogenous IFN-β, but not IFN-λ, protected MCs against HRV infection.
Conclusion And Clinical Relevance:
MCs are permissive for the replication and release of HRV, which is prevented by exogenous IFN-β treatment. Taken together, these findings suggest a novel mechanism whereby MCs may contribute to HRV-induced asthma exacerbations.
Insights
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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