Journal
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
Volume 4, Issue -, Pages -Publisher
FRONTIERS RESEARCH FOUNDATION
DOI: 10.3389/fcimb.2014.00002
Keywords
infection; nutritional immunity; iron; zinc; manganese; lipocalin-2; calprotectin; S100 proteins
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Funding
- Public Health Service Grants [AI083663]
- Pacific Southwest Regional Center of Excellence for Biodefense and Emerging Infectious Disease Research funds from the National Institute of Allergy and Infectious Diseases [U54AI065359]
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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.
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