Research Paper Volume 12, Issue 7 pp 6120—6128
Alveolar macrophage - derived exosomes modulate severity and outcome of acute lung injury
- 1 Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University, Shanghai 200433, China
- 2 Department of Respiratory Medicine, Shanghai Pulmonary Hospital, Tongji University, Shanghai 200433, China
- 3 Department of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, China
- 4 Department of Geriatrics, Zhongshan Hospital, Fudan University, Shanghai 200032, China
received: January 8, 2020 ; accepted: February 20, 2020 ; published: April 7, 2020 ;https://doi.org/10.18632/aging.103010
How to Cite
Copyright © 2020 Ye et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Severe acute lung injury (ALI) can cause death, and the survivals may develop acute respiratory distress syndrome (ARDS) due to fibrotic repair of the lung. Alveolar macrophages play a demonstrative role during the pathogenesis of ALI, and the timing and degree of differentially polarization of macrophages determine the severity of disease and outcome. Exosomes are important mediators of cellular communication and play critical roles during macrophage differentiation, proliferation and function. Nevertheless, the exact effects of alveolar macrophage - derived exosomes on ALI remain unknow. Here, we used lipopolysaccharide (LPS) to induce ALI in mice and analyzed the exosome population in bronchoalveolar lavage fluid (BALF) from macrophages, neutrophils and epithelial cells at different time points after treatment. Our data showed that macrophages were the major secretors for early secreted pro-inflammatory cytokines in the BALF-exosomes, which likely activated neutrophils to produce a variety of pro-inflammatory cytokines and IL-10. IL-10 by neutrophils in BALF-exosomes likely in turn polarized macrophages to M2c, which may be responsible for post-ALI fibrosis. Our study thus reveals a previous non-acknowledged role of BALF-exosomes as a mediator of inflammatory response and cell crosstalk during ALI.