Respiratory viruses such as rhinoviruses can exacerbate allergen-driven asthma. In Science Translational Medicine, Beale et al. report that patients with atopic asthma produce more IL-25 in response to infection with rhinovirus than do healthy people, which contributes to the severity of allergic inflammation and airway hyper-reactivity. Infection with rhinovirus also enhances the production of IL-25 by bronchial epithelial cells in mouse allergy models. This response correlates with greater production of type 2 cytokines, enhanced recruitment of leukocytes and accumulation of cells expressing IL-17RB (the IL-25 receptor) in the infected lungs. However, such allergen-sensitized mice have higher viral loads in their airway tissues, which suggests that this response interferes with antiviral immunity. Blocking IL-17RB in the mouse lungs relieves the exacerbation of asthma and diminishes the viral load. Thus, targeting IL-25 signaling pathways may have therapeutic effects that lessen the disease severity and morbidity associated with viral exacerbation of asthma.

Sci. Transl. Med. 6 (1 October 2014) doi:10.1126/scitranslmed.3009124