Role of complement in host defense against experimental disseminated candidiasis.
The role of complement in experimental disseminated candidiasis was studied in normal guinea pigs, animals congenitally deficient in the fourth component of complement (C4), and animals depleted of alternative pathway activity by cobra venom factor (CVF). Animals pretreated with CVF and challenged with Candida albicans had a high rate of mortality. Results of quantitative organ cultures corroborated prior reports that the kidney was the major target organ of infection. Infection of the kidney was markedly enhanced by CVF-induced depletion of the alternative pathway but not by classical pathway deficiency (deficiency in C4). There were differences among organs (kidney, liver, and spleen) in their requirement for complement to mount an effective host defense response. Ultimately, the integrity of the alternative pathway and late components of complement appears necessary for the limitation of and survival from sepsis due to C. albicans in nonimmune animals.
D000818:Animals; D002176:Candida albicans; D002177:Candidiasis / Q000276:immunology* / Q000401:mortality; D003166:Complement Activating Enzymes / Q000172:deficiency; D003181:Complement C4 / Q000172:deficiency; D003165:Complement System Proteins / Q000502:physiology*; D004546:Elapid Venoms / Q000276:immunology; D006168:Guinea Pigs; D007111:Immunity, Cellular; D007113:Immunity, Innate; D007668:Kidney / Q000276:immunology; D008099:Liver / Q000276:immunology; D008297:Male; D013154:Spleen / Q000276:immunology
D003181:Complement C4; D004546:Elapid Venoms; D003165:Complement System Proteins; D003166:Complement Activating Enzymes