Abstract
Human serum inhibits the growth of a variety of microorganisms, including many pathogens. To a large extent, bacteriostasis is due to serum transferrin (Tr), which binds iron tightly, making it unavailable to bacteria which require the metal for nucleoprotein synthesis and growth. Addition of exogenous iron to serum abolishes its bacteriostasis. Weinberg's hypothesis of “nutritional immunity” postulates that unsaturated Tr is protective against infection and cautions that iron treatment might reduce host resistance by increasing serum iron. In most reported studies, iron has been added to serum in vitro rather than employing sera with varying intrinsic iron contents. We confirmed that normal heat-treated human serum inhibited growth of two pathogenic E. coli isolates. Addition of iron to saturate Tr abolished the bacteriostatic properties. In contrast, we found no differences in the rates of growth of a standardized inoculum of E. coli in sera from 3 iron-deficient, 17 normal, and 13 iron-overloaded individuals (serum Fe 26-349 μg/dl, Tr saturation 6-100%). Iron added to serum in vitro is probably non-specifically bound to several proteins from which bacteria can easily extract it. However, in vivo, the metal is completely and firmly complexed to Tr and hence non-available. The contention that ordinary iron treatment predisposes children to infection is not supported by a body of epidemiological evidence. Our studies provide experimental data which cast further doubt on “nutritional immunity” as an important host defense mechanism.
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Pearson, H., Baltimore, R. & Shedd, D. 849 EFFECTS OF SERUM IRON AND TRANSFERRIN CN BACTERIOSTAS-IS: IN VIVO-IN VITRO DIFFERENCES. Pediatr Res 15 (Suppl 4), 584 (1981). https://doi.org/10.1203/00006450-198104001-00874
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DOI: https://doi.org/10.1203/00006450-198104001-00874
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