Taken together, there is evidence from various animal models that support a predominant role of C5a in initiating a cascade of inflammatory events during acute lung injury. If lung trauma is severe, activation of the innate immune system can lead to a dysregulated inflammatory response resulting in ARDS [125] . Elevated levels of C3a and C5a were measured in plasma of patients with ARDS [126] . In addition, experimental complement inhibition led to attenuated pathology in an animal model of lung injury [126] [127] [128] . Thus, it is tempting to speculate that C5a might act as a potential target for immunomodulation after chest trauma [74] , to avoid the deleterious effects of posttraumatic inflammation, which lead to ARDS, multiorgan failure, and death [97, 129] .