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 Le Bonheur research published in the Journal of Leukocyte Biology.
“Very little is known about how eosinophils respond to direct exposure to IAV or the microenvironment in which the viral burden is high,” said Le Bonheur researcher Amali Samarasinghe, PhD. “We hypothesized that eosinophils would dynamically respond to the presence of IAV through phenotypic, transcriptomic and physiologic changes.”
Researchers investigated eosinophil characteristics in different niches in a mouse model of fungal asthma and influenza, as well as responses to in vitro IAV exposure.
Results of the study showed:
Overall, mice with fungal asthma that were protected from severe IAV morbidity had reduced levels of cytokines – which can contribute to pathology when present in excess.
When exposed to IAV, eosinophils initiate self-preservation mechanisms to survive viral infection, such as conserving energy by reducing transcription activity and mitochondrial respiration. Concurrently, they increase their ability to recognize IAV and induce epigenetic changes in CD8+ T-cells that initiate their differentiation into cytotoxic cells known to be a critical component of the antiviral response.
LeMessurier KS, Rooney R, Ghoneim HE, et al. Influenza A virus directly modulates mouse eosinophil responses [published online ahead of print, 2020 May 9]. J Leukoc Biol. 2020; 10.1002/ JLB.4MA0320-343R. doi:10.1002/JLB.4MA0320-343R
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