Interleukin-1β Promotes Epithelial-Derived Alveolar Elastogenesis via αvβ6 Integrin-Dependent TGF-β Activation

Abstract

These data support the hypothesis that IL-1β was initially induced by hyperoxia; αvβ6 subsequently interacted with and activated TGF-β1, acting as an epithelial/mesenchymal signaling molecule that contributed to excessive alveolar elastogenesis, the primary pathological feature of BPD.