Iron-dependency of biological properties of Candida albicans

Background: Candidal infections occur in individuals with humoral or cell immunity deficiency. Any disorders of iron metabolism promote immune deficiency and abnormal sensitivity to infections. Potential modification of biological properties of Candida spp. in disorders of iron metabolism has not been discussed. Aim: To clarify the effects of iron metabolism disorders on the modification of biological properties of C. albicans. Materials and methods: Growth kinetics of reference strain (24433 АТСС) and clinical isolates of C. albicans (n = 20) depending on the concentration of Fe2+ ions in the broth and serum of blood donors with various types of iron metabolism (n = 2) was studied by turbidimetry. We also assessed the expression of the adhesion gen (als3), hemolytic phospholipase C genes (plb1, plb2, plс) and aspartic protease gene (sap1) in serum of donors with various iron levels. Results: Growth parameters of all C. albicans strains studied depends on the iron levels in the medium. The calculated constant of affinity to Fe2+ (Ks) for C. albicans strains was in the range from 179.5 to 1863.3 μM. Clinical isolates are more iron-dependent (179.5 < Ks < 1000 μM), compared to the reference strain ATCC 24433 (Ks = 1199.5 ± 28.3 μM). The optimal concentration of iron for the growth in the broth is 30 to 50 μM. The serum from individuals with normal iron metabolism inhibits the growth activity of C. albicans and is associated with overexpression of all virulence genes studied. Incubation of C. albicans with iron-deficient and iron-loaded sera results in an increase in the growth rate up to 0.017 h-1 and 0.012 h-1, respectively, but is associated with a reduction in expression of the major virulence genes. Conclusion: Biological properties of C. albicans are modified depending on the iron metabolism of the host. In those with normal iron metabolism, immune system suppresses Candida growth. Excess iron levels may promote candidiasis, whereas in iron deficient states the outcome of infection depends on the immune status of the host.