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Iron, infection and immune function

A decrease in circulating Fe, or hypoferraemia, is one of the most constant features of infectious disease. Since Fe deprivation in bacterial cultures is regularly associated with inhibition of growth, it has been suggested that Fe deficiency may represent an important defence mechanism (Weinberg, 1990). The term ‘nutritional immunity’ has been introduced by Kochan (1973) to underline the importance of Fe deprivation as a key mechanism limiting the growth of invading organisms. Interleukin-1 (IL-l), a protein released by mononuclear phagocytes in response to microbial invasion, is a key mediator in the inflammatory reaction and is directly responsible for the hypoferraemia of inflammation (Dinarello, 1984). It enhances the synthesis of a number of acute-phase proteins such as fibrinogen, haptoglobin, ceruloplasmin, amyloid A protein and ferritin (Fig. 1). The result of increased ferritin synthesis is a block in Fe release resulting in reduced serum Fe levels. Because of the paucity of clinical information supporting the significance of Fe deficiency or overload in determining the severity of infectious disease in man, the nutritional immunity hypothesis has remained a topic of continued controversy (Hershko & Peto, 1988). This controversy is of more than academic interest, since both Fe deficiency and infectious diseases are common conditions, and Fe supplementation in some populations may resolve one problem while aggravating the other. In the text that follows, I shall discuss briefly the importance of microbial Fe requirements, the role of Fe