Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are complex syndromes with three overlapping phases characterized by the reduction of pulmonary compliance, disruption of the epithelial and endothelial barrier, and recruitment of inflammatory cells into the alveoli. However, how lung cells communicate with each other remains unclear.
This work uncovers a novel mechanism and functional significance of epithelium-immune cell crosstalk in response to noxious stimuli. Dr. Jin’s group was able to demonstrate that lung epithelial cell-derived extracellular vesicles (EVs) serve as key “signal transmitters” between the epithelium and alveolar macrophages. EVs are lipid bilayer-enclosed nanoparticles that are naturally released from a cell. Moreover, they were able to identify that caveolin-1, a membranous protein, is responsible for sorting microRNAs into EVs. MicroRNAs are small, highly conserved non-coding RNAs that are critical to regulate innate immune responses.
This study, providing insights into pathophysiological functions of lung cell-derived EVs and new directions for developing diagnostic/therapeutic approaches to ARDS, is published in the Journal of Experimental Medicine.