Abstract
Transition metal ions are essential micronutrients for all living organisms. In mammals, these ions are often protein-bound and sequestered within cells, limiting their availability to microbes. Moreover, in response to infection, mammalian hosts further reduce the availability of metal nutrients by activating epithelial cells and recruiting neutrophils, both of which release metal-binding proteins with antimicrobial function. Microorganisms, in turn, have evolved sophisticated systems to overcome these limitations and acquire the metal ions essential for their growth. Here we review some of the mechanisms employed by the host and by pathogenic microorganisms to compete for transition metal ions, with a discussion of how evading “nutritional immunity” benefits pathogens. Furthermore, we provide new insights on the mechanisms of host-microbe competition for metal ions in the mucosa, particularly in the inflamed gut.
Highlights
Transition metal ions are involved in many biological processes crucial for sustaining life
Neutrophils play a key role in nutritional immunity because they constitute the largest proportion of circulating white blood cells in humans, quickly mobilize to sites of infection, and express high levels of antimicrobial proteins that sequester metal ions, including lipocalin-2, lactoferrin, and, as detailed below, calprotectin (Masson et al, 1969; Steinbakk et al, 1990; Goetz et al, 2002)
In addition to the role of these metals in essential cellular functions, evidence is mounting that specialized mechanisms of zinc and manganese acquisition contribute to bacterial pathogenesis; for instance, zinc and manganese are important cofactors in neutralizing reactive oxygen and nitrogen species, suggesting an important role for these metals in resisting these types of host antimicrobial responses (Lynch and Kuramitsu, 2000; Bowman et al, 2011)
Summary
Transition metal ions are involved in many biological processes crucial for sustaining life. In response to infection, mammalian hosts further reduce the availability of metal nutrients by activating epithelial cells and recruiting neutrophils, both of which release metal-binding proteins with antimicrobial function.
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