It is well known that the pathogenesis of ALI is mediated by pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and high-mobility group box (HMGB) 1, which are released from macrophages, neutrophils and other cells of the innate immune system [3,4]. Here, TNF is linked to acute respiratory distress syndrome.