Eosinophils residing in the airways of mice respond to influenza A virus (IAV) infection through alterations in surface expression of various markers necessary for migration and cellular immunity responses, according to research published in the Journal of Leukocyte Biology by researchers from Le Bonheur Children’s Hospital and the University of Tennessee Health Science Center.
Previous research explored the effects of IAV infection in patients with allergic asthma. During the 2009 influenza pandemic, patients hospitalized with influenza experienced lower morbidity if allergic asthma was an underlying condition. In mice, the researchers reported that the beneficial effect of this co-morbidity correlated with a dramatic increase in eosinophils in the airways, which is a hallmark of allergic asthma. Eosinophils were susceptible to IAV infection and also presented IAV antigens to CD8+ T-cells which are heavily involved in resolving viral infections. This implied that eosinophils actively contribute to the antiviral response during influenza. While once considered to be a cell that degranulated after allergen encounters and incidentally promoted host pathology during allergy, this research contributed to expand the role of eosinophils to that of anti-viral mediators and specifically showed that eosinophils are active participants in the resolution of influenza. Many of processes that cumulate in eosinophils making this valuable contribution are unclear.