The complement system is part of the host defense with a number of biological effects, most of which contribute to the inflammatory reaction by activation of cells like leukocytes and endothelial cells. An intact complement system is required for protection against infection and for maintaining internal inflammatory homeostasis. However, the system is a double-edged sword as improperly or uncontrolled activation is disadvantageous and potentially harmful for the host. Meconium aspiration syndrome (MAS) is associated with a local inflammatory reaction in the lungs, frequently described as a chemical pneumonitis. Cytokines, arachidonic acid metabolites and reactive oxygen species are involved in this reaction. We have recently documented that meconium is a potent activator of complement in vitro and in an experimental piglet model of MAS, the latter presenting with an inflammatory profile closely resembling systemic inflammatory response syndrome. We postulate that complement activation may contribute to the pathogenesis of MAS.