Fig. 1

RV infection produces robust remodeling signatures in airway epithelia that are enhanced with asthma. (A) The healthy airway epithelial layer is composed of ciliated pseudostratified epithelial cells, goblet cells, neuroendocrine (NE) cells, club cells, and other epithelial cell subtypes that contribute to the overall maintenance of barrier protection and integrity. (B) Rhinovirus infection of healthy airways is facilitated by viral receptors on pseudostratified airway epithelia. Infected cells produce proinflammatory type 1 and type 2 cytokines and chemokines, as well as angiogenic soluble factors that are released into the sub-epithelial space. RV infection increases goblet cell number and mucus production and reduces the number of ciliated cells. Epithelial-to-mesenchymal transition (EMT) can be promoted by RV exposure, resulting in morphological changes in epithelial composition. Extracellular matrix (ECM) components and matrix metalloproteinases (MMPs) are upregulated by epithelial cells in response to RV. (C) RV infection in the backdrop of existing asthma results in exaggerated responses by airway epithelia, in part due to higher levels of type 2 cytokines, including IL-13. Infected asthma epithelia highly produce type 2 cytokines and chemokines, including IP-10, IL-25, IL-33, and TSLP. Goblet cell number and mucus production are highly enhanced and ciliated cell number is significantly reduced. EMT is induced by RV infection at higher rates in asthma airway epithelial cells. ECM and MMP activity are also highly upregulated in RV infection with asthma. Created with BioRender.com