CCL2 and acute respiratory distress syndrome: After being activated, PMVECs can produce a variety of inflammatory mediators, such as monocyte chenotactic protein-1 (MCP-1), interleukin-6 (IL-6), interleukin-8 (IL-8) etc. All these pro-inflammatory mediators can influx into the blood vessels and alveolar spaces directly or through the recruitment of other inflammatory cells, and then aggravate the damage of endothelial cells, resulting in the pathological changes of ALI/ARDS [5].