Iron status, immune response and susceptibility to infection.
Nutritional factors can modulate immune responses. The concentration of iron, amongst other nutrients, influences host defence mechanisms. In experimentally induced iron deficiency in animals, morbidity and mortality on bacterial challenge are increased several-fold. Cell-mediated immunity and intra-cellular bacterial killing by polymorphonuclear leucocytes are impaired in iron-deficient individuals. This impairment is likely to be mediated by the effect of iron lack on cell proliferation, DNA synthesis and activity of iron-containing and iron-dependent enzymes involved in killing and elimination of microbes. Conversely, the availability of the free iron is a critical determinant for bacterial multiplication. It is not surprising then that epidemiological and clinical data on the frequency of infections--bacterial, fungal and others--in iron-deficient, iron-overloaded and healthy groups differ so widely. Vulnerability to infection based on the individual's iron status must be the net result of the effect of iron, or the lack of it, on microbial growth on the one hand and on immunocompetence of the host on the other. The key to keeping these interactions within physiological bounds is 'optimal iron nutrition'.
D000747:Anemia, Hypochromic / Q000150:complications / Q000276:immunology*; D000917:Antibody Formation; D001424:Bacterial Infections / Q000150:complications / Q000276:immunology; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007136:Immunoglobulins / Q000032:analysis; D007502:Iron Chelating Agents / Q000502:physiology; D007732:Kwashiorkor / Q000150:complications; D008214:Lymphocytes / Q000276:immunology; D008297:Male
D007136:Immunoglobulins; D007502:Iron Chelating Agents