Abstract

The hypothesis that iron repletion may enhance parasite multiplication and aggravate malaria infection in iron-deficient hosts was tested in a murine model of dietary iron deficiency and iron supplementation. Weanling C57Bl/6J mice were fed diets containing either 15mg iron/kg diet (Group D, n=20) or 50 mg iron/kg diet (Group N, n=12). After 30 days, when hemoglobin levels (Hb in g/100ml; Mean ± SD) were significantly lower in Group D (13.7 ± 1.2) than in from Group N (15.4 ± 2.0), 16 mice from Group D and 8 mice from Group N were inoculated intraperitoneally with 10 4 intraerythrocytic Plasmodium chabaudi (AS strain) malaria parasites. Four animals from each group remained as non-infected controls. At the time of inoculation, 8 mice from Group D (thereafter Group DS) and all animals from Group N (thereafter Group NS) were transferred to a diet containing 140 mg iron/kg, whereas 8 mice from Group D were maintained on the original iron-deficient diet. At the peak of parasitemias (day 10–11 post-infection), anemia was less severe in mice from Group DS if compared to those from Group D (Hb: 4.5 ± 1.1 vs. 3.4 ± 1.0), but more severe than in those from Group NS (5.6 ± 1.8). However, the time course of parasitemias was similar in all groups. Mortality was higher among mice from Groups D and DS (87.5%) than in those from Group NS (37.5%; Fisher's exact test, p = 0.0104). These data indicate that neither iron deficiency suppressed nor iron repletion enhanced P. chabaudi multiplication in weanling mice. Moreover, dietary iron supplementation induced hemoglobin response in iron-deficient mice but did not increase their ability to resist severe malarial anemia.

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