The Relationship of Transferrin and Iron to Serum Inhibition of Candida Albicans

Abstract

An intriguing property of human transferrin, a normally occurring beta globulin, is its ability to inhibit the growth of various organisms pathogenic to man (1, 2). This non-specific effect is most likely related to its affinity for iron and the ease with which, by alteration of physiologic conditions, iron binding can be reversed. Whereas the degree of bacteriostasis of Staphylococcus aureus grown in human serum can be inversely correlated with the percentage of iron saturation, other organisms (e.g. Staphylococcus albus) show no growth unless iron is provided in excess of the amount required to saturate transferrin. Serum from agammaglobulinemic patients has both a higher level of heat stable bacteriostatic activity against Bacillus subtilis and an increased unsaturated iron binding capacity (UIBC) compared to normal serum (3). This finding suggested that the increased levels of unsaturated transferrin may represent a compensatory defense mechanism in the agammaglobulinemic host. The addition of purified human transferrin to tissue culture media has also been shown to cause marked suppression of the cytopathogenic effect of several types of virus (4).