TNF and acute respiratory distress syndrome: A unifying hypothesis is that aberrant inflammation and EC activation (see Section 2) drive neutropenic ARDS pathogenesis, validated in mice sequentially depleted of circulating neutrophils [anti-Ly6G monoclonal antibody (mAb)] and separately neutrophils/monocytes (anti-Gr1 mAb) that generate stepwise and paradoxical TNF-α hyperinflammatory responses to endotoxin (133).