A mechanism for decreased resistance to infection by gram-negative organisms during acute alcoholic intoxication.
The propensity of alcoholics to develop infections with gram-negative bacteria is well known. However, the known effects of ethanol on host-defense mechanisms do not explain this tendency satisfactorily. Since the principal defense mechanism against gram-negative bacteria is their destruction by complement in the presence of specific antibody, we investigated the effect of acute ethanol intoxication on serum complement concentrations and correlated these with serum bactericidal activity against a gram-negative organism. Serial measurements of total hemolytic complement (CH5O) and C'3, ethanol concentration, and serum bactericidal capacity were performed on the serum of 7 dogs infused with a 10 per cent ethanol solution. All animals showed a substantial decrease in total hemolytic complement activity which was inversely related to the increase in serum ethanol concentration. A decrease in serum bactericidal activity correlated with the decrease in CH50. Control animals showed no variation in either CH50 or serum bactericidal activity. Immunoprecipitation studies, using antibody to dog C'3, indicated that serum concentrations of this protein were not altered by infusing the animals with ethanol. Incubation of serum in vitro with both ethanol and acetaldehyde had no effect on CH50. We conclude that the effect of ethanol on serum complement is an in vivo phenomenon probably relating to decrease in the synthesis of one or more of the components of complement other than C'3, although the formation of an anticomplementary substance cannot be excluded. These findings are presented as a possible explanation for the development of infections with gram-negative bacteria in ethanol-intoxicated subjects.
D000079:Acetaldehyde / Q000494:pharmacology; D000435:Alcoholic Intoxication / Q000276:immunology*; D000437:Alcoholism / Q000150:complications / Q000276:immunology; D000818:Animals; D001419:Bacteria / Q000276:immunology*; D001424:Bacterial Infections / Q000276:immunology*; D001770:Blood Bactericidal Activity / Q000187:drug effects*; D003176:Complement C3 / Q000096:biosynthesis; D003169:Complement Inactivator Proteins; D003165:Complement System Proteins / Q000096:biosynthesis; D003864:Depression, Chemical; D004195:Disease Models, Animal; D004285:Dogs; D004927:Escherichia coli Infections / Q000276:immunology; D000431:Ethanol / Q000494:pharmacology*; D006801:Humans; D007106:Immune Sera; D005779:Immunodiffusion
D003176:Complement C3; D003169:Complement Inactivator Proteins; D007106:Immune Sera; D000431:Ethanol; D003165:Complement System Proteins; D000079:Acetaldehyde