IL33 and atopic asthma: The IL-33 and HMGB1-rich cytokine microenvironment that occurs as a consequence of airway epithelial cell death skews the ensuing inflammatory response toward a type-2 response, leading to increased ASM growth in early-life and potentially long-term changes in both resident airway cells and immune cells necessary for progression to a non-atopic asthma-like phenotype following viral challenge in later-life.