Inflammation is closely linked to the pathogenesis of ALI. Levels of Interleukin (IL)-8 and IL-1 have been found increased in the lungs of ALI patients (33, 34) and the persistent increase of inflammatory cytokines in the lung correlated with poor outcome in ALI (35) (36) (37) . Inflammatory mediators exert several effects on PMNs. For example, complement protein C5a activates PMNs, thus contributing to their pulmonary sequestration and mediating lung tissue injury (38, 39) . Several inflammatory mediators, including complement, cytokines, chemokines, and lipid mediators also are able to induce the expression of surface molecules on the endothelium, which further promote PMN recruitment (40, 41) . Tumor necrosis factor (TNF)-α and IL-1β are two important cytokines that are found regularly in the BALF of ARDS patients (36, 42, 43) at higher concentrations than in their plasma, thus supporting their local origin (35, 44) . However, anti-TNF and anti-IL-1 therapies have failed to protect septic patients from ALI (44, 45) . Proinflammatory cytokines also are regularly expressed by activated PMNs traveling to the lung (32) . They appear to be a relevant source of IL-1β, favoring the subsequent release of other mediators, such as TNF-α, MIP-2, and IL-8 (46) (47) (48) . However, an early anti-inflammatory response driven by IL-1-, TNF-and IL-6-receptors, with early peaking IL-10 levels, was also shown in ARDS patients (41) . In addition, PMN stimulation with lipopolysaccharide (LPS) or TNF-α showed an activation of nuclear factor kappa B (NF-κB), p38, and AKT (49, 50) . The degree of nuclear translocation of NF-κB in peripheral PMNs from patients with septic ALI was linked to ventilator time and survival (50) .