Low Dietary Boron Reduces Parasite (Nematoda) Survival and Alters Cytokine Profiles but the Infection Modifies Liver Minerals in Mice ,

Abstract

Although boron (B) is an essential trace mineral, any interactions that it may have with gastrointestinal (GI) nematode infections are unknown. This study explored whether low dietary B would: 1) alter survival or reproduction of Heligmosomoides bakeri (Nematoda); 2) modify the resulting cytokine response to this parasitic infection; or 3) influence liver mineral concentrations in the infected host. Balb/c mice were fed either a low-B (0.2 microg B/g), marginal (2.0 microg B/g), or control (12.0 microg B/g) diet. Diets commenced 3 wk before a primary infection and were fed for 4 wk (primary infection protocol) and 8-9 wk (challenge infection protocol). Mice were killed 6 d post-primary infection (d6ppi), or dewormed then reinfected (challenge infection protocol) and killed 14 or 21 d post-challenge infection (d14pci or d21pci, respectively). Low and marginal dietary B intakes impaired survival of the parasite, reduced intestinal inflammation, and modulated a broad range of cytokines and chemokines despite similar liver B concentrations in diet groups. Compared with control mice, cytokine production was lower following low and marginal B intakes at d6ppi but was elevated at d21pci. Serum alkaline phosphatase was higher at d6ppi than at d14pci and d21pci. Compared with d14pci, liver zinc, iron, and B concentrations were reduced at d21pci when worm numbers were also lower, whereas concentrations of sodium, potassium, molybdenum, chromium, and sulfur were higher. This study shows that parasite survival and cytokine and inflammatory responses are modified by dietary B intake but indicates that a GI nematode infection alters liver mineral concentrations.

Tissue Mineral Distributions are Differentially Modified by Dietary Protein Deficiency and a Murine Nematode Infection

“…Leptin is considered as a proinflammatory Th1 cytokine as it up-regulates IFN-γ production as well as a variety of other Th1 cytokines [30]. Thus, we suggest, based on the recent publications from our laboratory using similar diet and infection protocols [5,[11][12][13], that the shift from the required Th2 immune response to a more dominant Th1 response may be responsible for mineral redistributions in our PD H. bakeri-infected mice.…”

“…One aim of this paper was to explore whether protein deficiency modulated tissue mineral concentrations in infected mice, under conditions where dietary intakes of minerals exceeded recommendation and tissue concentrations were within normal range for the mouse [5,7]. We observed an intriguing redistribution of tissue minerals as a consequence of both H. bakeri infection and dietary protein deficiency despite adequate mineral intakes.…”

“…Redistribution of tissue minerals during GI nematode infection [1][2][3][4][5] has been partly attributed to inflammatory responses [1,5], whose activation is mainly dependent on Th2 cytokines IL-4 and IL-13 [28]. Other research has emphasized the impact of protein deficiency on cytokine profiles and the ratio of Th1 to Th2 cytokines [29].…”

“…Other altered mineral concentrations associated with GI nematode infections include reduced blood zinc in whipworm infection [2] and reduced blood copper in sheep infected with either Trichostrongylus [3] or with Haemonchus [4]. The possibility that GI nematode infection might lead directly to mineral redistributions has been suggested recently as Bourgeois et al [5] showed that Heligmosomoides bakeri infection altered concentrations of a wide range of liver minerals, including iron, zinc, calcium, phosphorus, potassium, sodium, and sulfur, despite adequate dietary intakes of these minerals. Suggested reasons for changes in mineral concentrations in infected animals have included reduced food intake, impaired digestion and absorption, and parasite-induced immune responses and associated metabolic activities [6].…”

Calorie restriction and susceptibility to intact pathogens

“…Trace minerals, elements and vitamins also can affect parasite establishment and survival (Koski and Scott 2003;Rivera et al 2003;Bourgeois et al 2007), both when they are limited, and when they exceed normal levels. Few parasitological studies have separated the effects of CR from those of deficiency of micro-or macro-nutrients that are often imposed by using food restriction protocols (but see Shi et al 1998;Koski et al 1999).…”