S ummary . Experimentally induced acute inflammation in rats is associated with a fall in plasma iron and iron‐binding capacity. Transferrin synthesis by the liver of these animals is normal and not increased in the presence of a low serum iron, as it is in iron deficiency. Human splenic macrophages and rabbit pulmonary macrophages which were maintained in culture for up to 1 week showed an ability to take up protein‐bound iron and labelled plasma proteins into the cytoplasm. It is suggested that the macrophage may be the site both of iron sequestration and of transferrin degradation. This would provide a unified hypothesis to account for the finding of a low serum iron and TIBC in inflammatory disorders.
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O’Shea et al. (1973) studied this question.