Hui-Hui Jie,1,2 Wei-Hua Lu1,3 

1Department of Critical Care Medicine, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu, Anhui, 241001, People’s Republic of China; 2Graduate School of Wannan Medical University, Wuhu, Anhui, 241001, People’s Republic of China; 3Anhui Province Clinical Research Center for Critical Respiratory Medicine, Wuhu, Anhui, 241001, People’s Republic of China

Correspondence: Wei-Hua Lu, Department of Critical Care Medicine, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), No. 2 Zheshan Road, Wuhu, Anhui, 241001, People’s Republic of China, Tel +86-13955370637, Email lwh683@126.com

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.

Keywords: sepsis, C—C motif chemokine ligand 2, CCL2, exosome, lung macrophages, acute lung injury