The basic injury of ALI is the destruction of the pulmonary capillary endothelium and alveolar epithelium by polymorphonuclear neutrophils (PMNs) and activated macrophages which constitute a source of numerous inflammatory mediators, including tumor necrosis factor (TNF)-α, interleukins (IL-1β and 6), and arachidonic acid (AA) and oxygen metabolites [16,17]. Here, TNF is linked to acute respiratory distress syndrome.