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Human mast cell interferon responses and survival in the context of Coronavirus and Respiratory Syncytial Virus are enhanced by IL-5

ABSTRACT: Mast cells have been shown to be important sentinel cells in multiple models of viral and bacterial infection. Exacerbations of allergic asthma and asthma deaths are often associated with respiratory viral infections. Elevated levels of type 2 cytokines, especially interleukin 5 (IL-5), are also associated with allergic disease and have been targeted therapeutically. Here, we demonstrate that IL-5 signaling enhances the ability of human mast cells to mount a potent anti-viral response against respiratory viruses. Mast cells derived from umbilical cord-blood, treated with IL-5 and infected with respiratory viruses such as the human Coronavirus OC43 or respiratory syncytial virus (RSV) produced significantly more type I and type III interferons (IFNs) than non-IL-5 treated controls. IL-5 treatment also led to greater expression of IFN stimulated genes and upregulated expression of the pro-survival factor B-cell lymphoma 2 (BCL2) and protected mast cells from apoptosis-induced stress. IL-5 also upregulated expression of Endothelial PAS Domain Protein 1 (EPAS1), demonstrating an important IL-5 driven pro-survival network in mast cells. These resultssuggest an unexpected role for IL-5 signaling in regulating mast cell interferon responses and maintaining mast cell populations during mucosal viral infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE262880 | GEO | 2025/03/17

REPOSITORIES: GEO

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Project description:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ¬± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls. 38 samples classified in 4 categories : 14 isolated rhinitis (R), 6 rhinitis with uncontrolled asthma (UA), 7 rhinitis with controlled asthma (CA) and 11 healthy subjects (C )

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Human mast cell interferon responses and survival in the context of Coronavirus and Respiratory Syncytial Virus are enhanced by IL-5

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