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The research investigated the combined effects of protein deficiency (PD) and a gastrointestinal nematode infection, Heligmosomoides bakeri , on immunopathology and nutritional status in BALB/c mice. The acute phase of a primary infection reduced resting metabolic rate, but PD did not. Early challenge infection led to temporary anorexia and cessation of weight gain in both protein-sufficient (PS) and PD mice. / Among PS mice, a challenge dose of 200 L3 caused more active worm expulsion than infection with 100 L3. Both serum monocyte chemotactic protein-5 and gut fluid leakage were positively correlated with worm expulsion whereas numbers of mucosal mast cells, eosinophils, goblet cells and Paneth cells were unaffected by doses. Among PD mice, worm survival was prolonged and no dose-dependent worm expulsion was observed. In addition, a wide range of Th1 inflammatory cytokines including leptin was elevated in infected PD mice suggesting (1) that PD mice are unable to mount the appropriate Th2 inflammation and (2) that infection in PD mice induces a Th1 inflammation that allows continuing persistence of the parasite. / The shift to Th1 inflammatory responses in PD mice may also explain modifications in mineral distributions in tissues. Despite adequate dietary intakes of minerals in both PD and PS mice, serum iron concentrations were lower after H. bakeri challenge infection. Infection also reduced calcium and iron concentrations as well as the Ca/Zn ratio in the spleen. In contrast, PD resulted in increased iron and calcium concentrations as well as increased Ca/Zn ratio in the spleen and Fe/Zn ratio in the liver, but reduced calcium, zinc, copper and sulfur concentrations, and the Cu/Zn ratio in the liver. / Re-feeding PD mice with a PS diet restored parasite expulsion, regardless of whether the PS diet was provided during the primary or challenge infection. Thus, although PD mice have suppressed Th2 responses and elevated Th1 inflammation, their response to the primary infection is sufficient to ensure that parasite expulsion occurs once protein status is restored. / Together, these studies show that the shift toward Th1 inflammation plays a key role in prolonged parasite survival and mineral redistribution in protein deficient, infected mice.

The aim of this research was to determine the influence of iron deficiency on both the efficacy and metabolic patterns of albendazole in mice infected with Heligmosomoides polygyrus. Anthelmintic efficacy was markedly decreased in iron-deficient mice; the deficiency was also associated with a decrease in body weight, altered hematological parameters and a decreased net egg output; worm establishment in the deficient group was not affected by the deficiency. Although anthelmintic efficacy was significantly decreased by the iron deficiency, plasma concentration profiles of the main metabolites, albendazole sulphoxide and albendazole sulphone, were not changed by the deficiency. Levels of intestinal cytochrome P-450, the main metabolizing enzyme of albendazole however, was significantly depressed in iron-deficient mice. These observations suggest that although pharmacokinetic parameters are not affected by iron deficiency, nutritional status has the potential to influence anthelmintic efficacy and thus warrants further study.

In the past 20 years, boron has been identified as an essential trace element for animals and humans but also as an increasingly important industrial pollutant. We examined first whether boron influenced survival of the gastrointestinal nematode Heligmosomoides bakeri. Female Balb/c mice were fed deficient (0.1 mug B/g), marginal (2.0 mug B/g) or control (12.0 mug B/g) diets, and infected with third-stage larvae. Although liver boron concentrations did not differ among diet groups, dietary boron deficiency impaired survival of the parasite and modulated a broad range of cytokines and chemokines. On the other hand, infection history altered liver mineral concentrations. Second, we examined whether elevated boron concentrations would exert toxic effects on H. bakeri in vitro. Boron toxicity was evidenced by reduced motility, fecundity, infectivity and survival. Feeding stages and free-living stages were more sensitive than non-feeding stages and parasitic stages respectively in a dose-dependent manner.

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