Candidemia in humans is often associated with an endotoxic shock-like syndrome, comparable to gram-negative sepsis. Tumor necrosis factor-α (TNFα) has been implicated as a mediator in the endotoxic shock syndrome. The possible role of TNFα causing early deaths was explored in a murine model of acute infection with Candida albicans. In vitro data from three mouse strains (BALB/c, C3H/HeJ, and C3H/HeN) and in vivo data from BALB/c mice were obtained. Peritoneal macrophages from all three strains produced TNFα in vitro when stimulated with C albicans. After intravenous infection with 108 cfu of C. albicans, mice died within 12 h. TNF concentrations in sera from these mice were significantly greater than in controls. Pretreatment ofBALB/c mice with anti-murine TNFa did not alter mortality of C. albicans-infected mice, but pretreatment with murine TNFα reduced mortality. Therefore, in contrast to what was anticipated, TNFα may serve a protective role in murine candidiasis.
ASJC Scopus subject areas
- General Medicine