Clearance and killing of Candida albicans in the perfused mouse liver.

Hepatic interactions of C. albicans with perfused mouse livers were characterized and compared in normal and glucan-treated mice. Normal livers, in the absence of serum, trapped greater than 90% and killed greater than 20% of the infused yeast. Phenylbutazone had no effect. Silica treatment abolished killing and decreased trapping suggesting that candidicidal activity of the liver is mediated by Kupffer cells. Immune serum, but not normal serum, enhanced trapping and killing in normal livers. Liver hypertrophy was evident in mice treated with glucan, but no enhanced candidicidal activity was observed in the absence of humoral factors. Specific immune serum and normal serum increased killing of C. albicans in glucan stimulated liver, suggesting a requirement for serum opsonin in facilitating glucan enhanced killing. Specific immune serum potentiated the greatest increase in killing. Glucan treatment in conjunction with immune serum increased killing to approximately 40%. D-mannose, but not D-glucose or D-mannitol impaired trapping of the yeast in livers of normal mice. Together, the data suggest that hepatic trapping of C. albicans involves phagocytic events as well as interactions of the yeast with surface receptors on sinusoidal cells and support the role for the liver in restricting hematogenous dissemination of C. albicans in the infected host.