The complement-induced pulmonary response after chest trauma has been suggested to depend on a delicate balance between pro-and anti-inflammatory transcription factors [111] . Alveolar macrophage activation is characterized by increased nuclear translocation of nuclear factor(NF)-B and activator protein-1 (AP-1) representing an initial event in the genesis of the inflammatory cascade [112, 122] . In contrast to NF-B and AP-1, the transcription factor STAT3 has emerged as a negative regulator of the inflammatory response [28] . Interestingly, C5a has been shown to be responsible for STAT3 activation in lungs and alveolar macrophages after immune complex-induced lung injury whereas no complement-dependence could be found for activation of AP-1 [122, 123] . STAT3 has been hypothesized to act as a transcriptional mediator for the anti-inflammatory cytokine IL-10, and might contribute to a negative feedback system in acute lung injury [28, 111, 124] . In addition to the above described "classic" lung injury models, a recent study has paid more attention to the immune response after experimental blunt chest trauma induced by a blast wave [104] . Flierl and colleagues reported complement activation after trauma-induced bilateral lung contusion in rats with C5a-dependent perturbations in neutrophil functions. Treatment with anti-C5a antibody abolished functional deficits in neutrophils and reduced intrapulmonary levels of leukocytes and of cytokines [104] .