Severe blunt chest trauma with associated pulmonary contusions is characterized by a robust inflammatory reaction which can result in exacerbated lung injury, acute respiratory distress syndrome (ARDS), multiple organ failure, and death [95] [96] [97] [98] [99] . Activation of alveolar macrophages and recruitment of neutrophils into the interstitial and alveolar compartments are followed by the release of an arsenal of proteinases and oxidants causing leakage of the pulmonary microvasculature and destruction of the alveolar epithelium [100] [101] [102] [103] . Various experimental models of lung injury could yield important insights into the critical role of complement activation products, particularly anaphylatoxin C5a, in the pathophysiology of trauma-induced lung inflammation and progressive alveolar injury [28, [104] [105] [106] . Elevated levels of C5a have been described in broncheoalveolar fluid samples from patients with acute lung injury [28, 107, 108] . When C5a was applied intratracheally in rats exposed to an IgG immune complex model, increased intrapulmonary generation of chemokines, accumulation of neutrophils and changes in vascular permeability could be detected [106] . The protective effects of anti-C5a were further corroborated by the observation that the antibody also suppressed release of tumor necrosis factor (TNF) into bronchoalveolar lavage [109] . Furthermore, C5a was shown to be required for TNF-dependent upregulation of intercellular adhesion molecule-1 (ICAM-1), an essential endothelial adhesion molecule required for neutrophil migration [109] . Czermak and colleagues demonstrated that both the in vitro and in vivo blockade of C5a led to significantly reduced production of CXC and CC chemokines [110, 111] .