Exosome Secretion Regulation in Mice with Acute Lung Injury.

PURPOSE

Acute lung injury (ALI) is a typical critical illness. Exosomes can regulate the development of pulmonary inflammation by modulating macrophage metabolism and behavior. During ALI, C-C motif chemokine ligand 2 (CCL2) is involved in the occurrence and maintenance of the inflammatory response, and the amount of CCL2 secreted by exosome increases. This study was aimed at investigating the role and mechanism of exosome -mediated CCL2 in sepsis-related ALI using a sepsis model in mice and rat type II alveolar epithelial cells. Furthermore, we explore the regulation of extracellular vesicle secretion in acute lung injury in mice.

METHODS

The sepsis group was pretreated with an exosome inhibitor to determine the extent of exosome release and alterations in inflammatory factors in the lung tissue. Furthermore, RLE-6TN cell-derived exosomes were cocultured with rat alveolar macrophages. Subsequently, an ALI rat model was constructed, and exosomes produced in vitro were injected into rats via the tail vein to detect the expression levels of inflammatory factors and elucidate macrophage polarization pathways.

RESULTS

After treatment with the exosome inhibitor, the number of exosomes and the expression of CCL2 in the lung tissue were significantly downregulated in the sepsis group. Exosomes secreted by lipopolysaccharide-treated rat type II alveolar epithelial cells stimulated the polarization of M1 macrophages, which resulted in morphological and functional changes.

CONCLUSION

Exosome Secretion Regulation in Mice with Acute Lung Injury.