Relative roles of burn injury, wound colonization, and wound infection in induction of alterations of complement function in a guinea pig model of burn injury.

Stimuli involved in induction of alterations of the complement system and production of circulating inhibitor(s) of phagocytic function of polymorphonuclear neutrophils following burn injury were investigated using a guinea pig model of scald burn injury. The activity of C1-C9, assessed by measurement of total hemolytic complement, was found to increase primarily in response to burn injury per se, whereas reduction in the activity of the alternative complement pathway was shown to develop in association with natural colonization and local burn wound infection with bacterial pathogens. Invasive burn wound infection induced experimentally with Staphylococcus aureus, Pseudomonas aeruginosa, or Candida albicans exacerbated this latter abnormality, caused consumption of C1-C9 activity, and was associated with appearance of serum factors that depressed phagocytosis of Escherichia coli 075 by peritoneal polymorphonuclear neutrophils. Thus injury and coexistent infection both play important roles in induction of humoral alterations of host defense associated with burn injury.