The role of complement in glucan-induced protection against septic shock.
Previous studies from our laboratory have shown that glucan will significantly enhance survival, decrease bacteremia, maintain reticuloendothelial function, and reduce histopathology in a murine model of gram-negative septic shock [1]. The present study was undertaken to evaluate the role of complement in glucan-enhanced protection against septic shock. AKR/J mice, which are congenitally C5-deficient, and ICR/HSD mice that were complement-depleted by treatment with purified cobra venom factor (CVF), were injected IP with glucan (50 mg/kg) on days 5 and 3 prior to IP challenge with 1 X 10(8) E. coli. Survival data indicated that glucan (p less than 0.05) increased survival in both C5-deficient and complement-depleted mice. Glucan prophylaxis resulted in a neutrophilic leukocytosis 8 h following E. coli challenge. However, glucan did not alter bone marrow proliferation. We conclude that, 1) glucan's protective effect on survival is not dependent on complement, 2) complement is not required for glucan-induced neutrophilic leukocytosis in this model, and 3) glucan does not enhance bone marrow proliferation in complement-deficient mice.
D000818:Animals; D001853:Bone Marrow / Q000473:pathology; D002455:Cell Division / Q000187:drug effects; D003182:Complement C5 / Q000172:deficiency*; D003165:Complement System Proteins / Q000172:deficiency / Q000502:physiology*; D004927:Escherichia coli Infections / Q000150:complications / Q000401:mortality; D005936:Glucans / Q000627:therapeutic use*; D007962:Leukocytes / Q000187:drug effects; D051379:Mice; D012772:Shock, Septic / Q000209:etiology / Q000517:prevention & control*
D003182:Complement C5; D005936:Glucans; D003165:Complement System Proteins