The EVs secreted from human hepatocytes attenuated the CCL4-induced ALI by inhibiting the recruitment of neutrophils to the liver via reduction of C-X-C motif chemokine ligand 1 (CXCL1) and CXCL2 in the liver and that of monocytes via reduction of chemokine receptor (CCR)-8 and CCR-9 in bone marrow (BM) cells possibly mediated by docosahexaenoic acid (DHA), thus producing potent anti-inflammatory and proresolutive lipid mediators, were enriched with EVs than with hepatocytes. Here, XCL1 is linked to acute respiratory distress syndrome.