Alterations in Host Responses to Experimental Candida Albicans Infections by Bacterial Endotoxin

Abstract

Some of the mechanisms responsible for endotoxin-induced resistance to experimental Candida albicans infection in mice have been investigated. Maximal protection has been demonstrated at 1 and 6 days after endotoxin and serum factors have been shown to be important in both. The enhanced resistance to candidiasis observed 1 day following endotoxin is primarily due to transferable serum factor(s). At this time, organisms are cleared from the blood stream at an increased rate. However, this effect does not appear to be due to either the presence of serum opsonins or enhanced function of the reticuloendothelial system. In animals given endotoxin 6 days previously, there is significantly less proliferation of C. albicans in the kidney, the prime target organ of this infection. Serum factors present in the blood of these animals inhibit the growth of C. albicans in vitro. Therefore, at least two, probably different, serum factors seem to be involved in endotoxin-induced resistance. These serum factors may also require as yet undefined cellular mechanisms to produce the effects that were noted.