Exosomal miR-107 Derived From Cigarette Smoking-Exposed Bronchial Epithelial Cells Aggravates Acute Lung Injury by Polarizing Macrophage to Proinflammatory Phenotype.

Exosomes are critical mediators of intercellular crosstalk and play significant roles in the progression of various diseases including acute lung injury (ALI). However, the specific role of exosomes in ALI remains largely unexplored. In investigation, we demonstrated that exosomes released from cigarette smoke extract (CSE)-exposed bronchial epithelial cells (BEAS-2B) facilitated M1 macrophage polarization. Notably, CSE exposure enhanced the production of miR-107 within these exosomes. Inhibition of miR-107 markedly reversed the M1 macrophage polarization and inflammatory responses in vitro and ameliorated lung injury in vivo. Furthermore, exosomal miR-107 was found to downregulate KLF4, thereby promoting M1 macrophage polarization and inflammation of macrophages. Collectively, these findings demonstrate that CSE-exposed BEAS-2B cells could induce M1 macrophage polarization via transmitting exosomal miR-107, and eventually ultimately contributing to the progression of ALI, indicating a potential therapeutic strategy for ALI.