Lung eosinophil recruitment during breakthrough influenza infection in vaccinated mice is non-pathological and correlates with protection.

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Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B564
Abstract ID: 4255

Presenting Author:
Lauren A Chang , PhD Student at Icahn Sch. of Med., Mount Sinai

Abstract:

Eosinophils are critical cells in Th2 immune responses and homeostasis. Lung eosinophilia after respiratory viral infection has been linked to aberrant Th2 responses like vaccine-associated enhanced respiratory disease, but has been decoupled from pathology in some models of respiratory viral infection, with or without prior vaccination. We characterized mouse lung eosinophils after a sublethal, vaccine-matched influenza challenge (breakthrough infection). Post-challenge, we observed CD101⁺ Siglec-F^hi lung eosinophils in mice that received trivalent inactivated influenza vaccine. This group did not have strong inflammatory cytokine expression, detectable viral titers, allergic levels of total IgE, severe lung pathology, goblet cell hyperplasia, or enhanced morbidity. In contrast, unvaccinated mice exhibited no eosinophilia, high viral titers, strong pro-inflammatory cytokine profiles, and significant pathology. Longitudinal analyses at days 1, 3, 7, 10, and 28 post-challenge revealed no overt Th2 cytokine signal in the lungs of breakthrough infection mice, suggesting that non-canonical mechanisms and cell circuits promoted lung eosinophilia in this model. Furthermore, lung eosinophils correlated with protection and not pathology in breakthrough influenza infection of mice. We are now investigating the phenotype and function of lung eosinophils in viral vaccination and immunity via adoptive transfer studies, RNA-seq, imaging, and high-dimensional spectral flow cytometry.