Increased in vitro tumour necrosis factor-alpha production in iron deficiency anemia.

In vitro monocyte-derived tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) production was assessed in iron deficient with anemia (IDA), iron deficient without anemia (ID) and control infants. The concentrations of released and cell-associated cytokines were measured before and after 3 months of iron supplementation in all groups (ferrous sulphate drops: 3 mg/Kg/day). No difference in released and cell-associated IL-1 beta was observed between either groups of infants. Lipopolysaccharide-stimulated blood mononuclear cells from IDA (n = 9) infants produced a significantly higher immunoreactive TNF-alpha concentration as compared to ID (n = 9) and normal subjects (n = 18) on admission (F = 6.72; p < 0.004). After iron therapy, the LPS stimulated TNF-alpha secretion by cells of IDA infants returned to the levels observed in the other groups. Since TNF-alpha plays a key role in iron metabolism, we speculate that increased TNF production in IDA infants could exacerbate the inhibition of erythroid proliferation present in these conditions. Further studies are needed to evaluate the effect of more severe anemia as well as to clarify the biological effect of increased TNF-alpha production in iron deficiency anemia and its consequences.