Stephania A. Cormier

TL;DR: It is suggested that degranulation of eosinophils recruited to the lung in this model does not occur at levels comparable to those observed in humans with asthma, and that EPO activities are inconsequential to the development of allergic pulmonary pathologies in the mouse.

TL;DR: RSV infection in neonates alone led to inflammatory airway disease characterized by airway hyperreactivity, peribronchial and perivascular inflammation, and subepithelial fibrosis in adults, and the data presented emphasize IL-13 and TNF-α as potential therapeutic targets for treating RSV induced-asthma.

TL;DR: CD4(+) T cell-mediated inflammatory signals as well as signals derived from eosinophils are each necessary, yet alone insufficient, for the development of allergic pulmonary pathology and suggest that eOSinophil effector functions impinge directly on lung function.

TL;DR: It is demonstrated that respiratory viral infection induces distinct fibroblast activation states, which are term extracellular matrix (ECM)-synthesizing, damage-responsive and interferon-responsive states, and evidence that excess activity of damage- responsive lung fibroblasts drives lethal immunopathology during severe influenza virus infection is provided.

TL;DR: It is argued the understated importance of utilizing infant models to truly understand the etiology of PM‐induced predisposition to severe, persistent lung disease, with a focus on the emerging importance of environmentally persistent free radicals ubiquitously present in combustion‐derived PM.