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The concept of nutritional immunity

Nutritional Immunity is a process by which an animal sequesters trace minerals in an effort to limit pathogenicity during infection. Circulating concentrations of minerals, such as iron, zinc, manganese, decline rapidly and dramatically at the site of infection associated with inflammation. The decline of these trace minerals is thought to starve invading pathogens of these essential nutrients, limiting disease progression and severity.


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Minerals are essential nutrients for both animals and pathogenic microbes. Because of their ability in several oxidation states, minerals are ideal redox catalysts for diverse cellular processes including respiration and DNA replication. In fact, approximately half of all proteins and enzymes require trace minerals to confer function.


Given the absolute requirement for minerals by virtually all pathogens, an important facet of the innate immune system is to limit minerals availability to invading microbes in a process termed “nutritional immunity”. Successful pathogens must therefore possess mechanisms to circumvent nutritional immunity in order to cause diseases.


In the diagram below, we illustrate the protection mechanism from the animal against the infection from a pathogen through the reduction of iron.


Hepcidin and transferrin limit the availability of free iron, thus affecting the ability of invading pathogens to replicate and cause disease. Animals also use the regulation of transporters, such as natural resistance-associated macrophage protein 1 (NRAMP1), to withhold iron from pathogens. NRAMP1 is localized in lysosomes and phagosomes of monocytes, macrophages, and T lymphocytes where it functions to export iron (and manganese) into the cytosol, thereby limiting the availability of iron to pathogens that enter the cell.


Similar mechanism has been demonstrated for Zinc and Manganese. Researches identified in large quantity in abscesses a protein called Calprotectin. Calprotectin is the most abundant antimicrobial protein in neutrophils, making up to 40% of the cytoplasmic neutrophil content, and is secreted at the site of inflammationevery time that hosts identify an infection. This protein has the properties to bind Zinc and Manganese ions. By depleting the abscesses of these minerals, the Calprotectin is actually limiting the development of the bacteria.


Experimentations made at Nashville University demonstrated that the addition of Zinc and Manganese in these abscesses was triggering the development of the Staphylococcus by neutralizing the depletion strategy intended by the immune mechanism described above.


By sequestering manganese and zinc, the Calprotectin plays a crucial role in the animal defense against bacterial and fungal pathogens. However, the essential processes disrupted by calprotectin remain unknown. One assumption is that calprotectin enhances the sensitivity of Staphylococcus aureus to superoxide dismutase through the inhibition of manganese-dependent bacterial SOD defenses, thereby increasing SOD levels within the bacterial cell.


Excess of metals in diet is actually disrupting the ‘Nutritional Immunity’. That prevents the organism to create the metal deficiencies that is required to fight against bacteria.


Recently, there has been a growing appreciation for the role of diet and dietary metal levels in impacting host-pathogen interactions and susceptibility to infections.


Recent research evidence indicates that pathogens have developed multiple mechanisms to overcome iron and zinc sequestration in response to infection and inflammation. For example, siderophores, low-molecular-weight (<1 kDa) iron-chelators, are secreted by pathogens and bind and chelate iron with a higher affinity than transferrin. Siderophore-iron complexes are then scavenged by pathogens via cell surface receptors and the bound iron is released inside bacteria to be used as nutrient. In fact, pathogenic strains that produce more siderophores are hypervirulent, whereas strains that synthesize defective siderophores are less virulent.


The strategy of reducing circulating trace minerals level is detrimental to a normal physiology of the host. But in acute situation, the nutritional immunity mechanisms will favor ‘defensive strategy’ versus basal physiology hoping that the situation comes back to normal before deficiencies appears in the other biological processes of the animals. Situation will become critical if the infection lasts too long.


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