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Severe asthma patients (SA) are more susceptible to respiratory infections with human rhinoviruses (HRV) than healthy subjects (H), causing exacerbations. In response to HRV, circulating immune cells are recruited to and activated at the local sites of infection. Hypothesis: The activation of circulating immune cells in response to HRV is impaired in severe asthma. We infected peripheral blood mononuclear cells (PBMC) of H (n = 20) and SA (n = 50) with RV-A16 ex vivo. Cytokines were measured in culture supernatants by ELISA. Data were compared between SA and H and correlated to asthma phenotype biomarkers. RV-A16 induced IFNα, IFNγ, CCL2, CCL5, TNFα, IL-1β, IL-6 and IL-8. Except for CCL2, these cytokine responses were reduced in SA versus H. In SA, IFNα, IL-6 and CCL5 responses correlated negatively, but IL-1β correlated positively to FeNO. IFNγ correlated positively to blood eosinophils and serum IL-33, and INFα correlated positively to serum total IgE. Cytokine responses of circulating immune cells to RV-A16 are reduced in SA. Cytokines are differentially affected in allergic, eosinophilic or T2 low asthma. This could help to explain the increased risk for exacerbations in HRV infections in severe asthma and differences between phenotypes. Circulating immune cells might be considered as drug targets to reduce exacerbation rates.
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Jameel et al. (2026) studied this question.
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