The role of iron in cell division and cellular functions is well established. Almost all living cells, including bacteria, fungi, protozoa, mammalian cells from various tissues (including those of the immune system) require iron for DNA synthesis and many other cellular functions (Cazzalo et al., 1990). In addition to its role for ribonucleotide reductase activity, iron is also a cofactor of enzymes involved in cell respiration, antioxidant defence (catalase) and neutrophil bacterial killing (myeloperoxidase). Microorganisms need iron in the concentration range of 22-220 ^g l-1 (Payne and Finkelstein, 1978). Although an insufficient supply of iron will diminish the growth of microorganisms (Patruta and Horl, 1999), the iron in human body fluids and tissues is potentially more than sufficient to sustain optimal growth of microorganisms (Fairbank, 1988; Cook and Skikne, 1989; Cazzalo et al., 1990). However, this iron is tightly bound to various proteins (haemoglobin, myoglobin, ferritin, lactoferrin, transferrin and various enzymes) and therefore is, in general, unavailable to microorganisms. On the host's side, too little iron may impair immune responses, especially those that require cell proliferation and bactericidal activity. Too much iron is toxic to cells, as it induces peroxidation of intracellular and cell-membrane macromolecules, and it may also impair immune functions. Thus, there must be a suitable amount of iron available to support immune function, while not promoting the growth of infectious agents above that with which the host defence can cope. The importance of this subtle balance probably explains the variety of observations that have been made with regard to the influence of iron status on susceptibility to infection. Some observations demonstrate that iron promotes infection, suggesting that iron deficiency is 'beneficial', as it may protect from infectious illnesses. Other observations show that iron protects from infection, which implies that iron deficiency is deleterious and may promote infection. Yet other observations indicate that iron status alone is probably insufficient to determine susceptibility to infection. Supporting data on each of these views exist in the literature and have been reviewed by other authors (Walter et al., 1997; Patruta and Horl, 1999).
Several studies have been published that suggest that iron may promote infections. For example, administration of iron, especially to neonates and schoolage children, increased various types of infection (Barry and Reeve, 1977; Murray et al., 1978a, b; Smith et al., 1989) and, in some studies, mortality was significantly increased (see McFarlane et al., 1970; Brock, 1993). In support of the idea that iron promotes infection is the observation that, during infection, the host responds by decreasing serum iron concentration and shifting it to storage in the reticuloendothelial cells; it may be that this is an attempt by the host to deprive the invading microorganisms of iron.
The situation regarding iron status and malaria is complicated by the fact that it is the red blood cell that is parasitized. The malaria parasite is totally dependent upon red blood cells of the host to complete its life cycle. This might explain the observations that malaria is more common in iron-replete than in iron-deficient individuals (Oppenheimer et al., 1986) and that the levels of malaria infection and the severity of disease were increased by iron supplementation (Murray et al., 1978a, b).
Evidence that iron may protect from infection and that iron deficiency may promote infection
Some studies have shown that prevention, as well as treatment, of iron deficiency by medicinal iron and food fortification reduces the rate of respiratory and non-respiratory infections (e.g. Chwang et al., 1988; Hussein et al., 1988).
Evidence that iron status alone may not determine susceptibility to infections
Several studies suggest that iron status does not affect susceptibility to infections (e.g. Snow et al., 1991; Heresi et al., 1995; Menendez et al., 1997). In a study, conducted in Tanzania, of more than 800 infants, iron supplementation for 24 weeks starting at 8 weeks of age did not significantly affect the rate of malarial infection (Menendez et al., 1997). Unfortunately, the rate of other types of infection was not reported. Iron fortification during the first year of life in Chilean children did not alter the rate of diarrhoeal diseases and respiratory infections (Heresi et al., 1995). In fact, the rate of infection was higher in children with iron deficiency compared with children with adequate iron status, regardless of iron treatment. However, it was unclear from the paper what came first, iron deficiency or infection.
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