The very early stage after tissue trauma is characterized by activation of cellular and molecular effectors of the innate immune system, including complement activation and recruitment and activation of neutrophils (polymorphonuclear leukocytes; PMNL) [6, 7] . The complement system appears to represent the crucial effector of innate immune responses in the early phase after major trauma [23] [24] [25] . Once the cascade is activated through one of three (five) established pathways (Figure 1 ), complement plays a critical role in the elimination of invading pathogens by opsonization for phagocytosis (C3b, C4b), chemotaxis of leukocytes (C3a, C5a), and by direct lysis of pathogens through the membrane attack complex (MAC, C5b-9) [23, 26, 27] . The generation of anaphylatoxins C3a and C5a provides potent chemoattractants for phagocytes and neutrophils, and recruit these immune cells to the site of injury [24, 28, 29] . The anaphylatoxins further induce degranulation of mast cells, basophils and eosinophils and mediate the hepatic acute-phase response [30, 31] . Finally, the generation of C5b by cleavage of C5 initiates the terminal complement pathway with MAC formation. The MAC forms through the self-association of C5b along with C6 through C9 and leads to the formation of a large membranolytic complex capable of lysing prokaryotic and eukaryotic cells [32] . Multiple previous studies have unequivocally shown that trauma activates complement, both locally at the site of injury, and systemically. Early studies in the 1980s revealed that the complement cascade is activated at the level of C3 in serum of trauma patients, and the extent of activation correlates with the severity of injury [33, 34] .