We speculate that SARS-CoV-2 infection in pulmonary epithelial cells induces IL-6 trans-signaling for secretion of chemokines; like MCP-1, from pulmonary vascular endothelial cells, and attract monocytes/macrophages to create a hyper-inflammatory state leading to pulmonary edema and a disturbance of oxygen exchange or acute respiratory distress syndrome. Here, CCL2 is linked to acute respiratory distress syndrome.