CXCL8 and acute respiratory distress syndrome: Subsequently to this early phase, the excessive virus replication in patients with ARDS promotes excessive IFN response associated with excessive production of inflammatory mediators, like interleukin-(IL)-1β, IL-6, tumor necrosis factor (TNF) α and neutrophil-recruiting chemokines (e.g., CXCL8/IL-8) [55,56] by immune and non-immune pulmonary cells.