Abstract
Iron is an essential nutrient for almost all living organisms, but is not easily made available. Hosts and pathogens engage in a fight for the metal during an infection, leading to major alterations in the host’s iron metabolism. Important pathological consequences can emerge from the mentioned interaction, including anemia. Several recent reports have highlighted the alterations in iron metabolism caused by different types of infection, and several possible therapeutic strategies emerge, based on the targeting of the host’s iron metabolism. Here, we review the most recent literature on iron metabolism alterations that are induced by infection, the consequent development of anemia, and the potential therapeutic approaches to modulate iron metabolism in order to correct iron-related pathologies and control the ongoing infection.
Highlights
The virulence of a pathogen is directly related to its capacity to adapt to the environment present within the host, and its ability to escape or subvert the host’s immune response
When infected with Vibrio vulnificus, Y. enterocolitica serotype O9 or Klebsiella pneumoni, a dramatic increase in pathogen growth and host mortality occurred in mice that were genetically deficient in hepcidin production [38,46,47]
Data from these experiments showed that hepcidin decreased the levels of circulating iron and especially non-transferrin bound iron (NTBI), which is critical to avoid the proliferation of highly siderophilic bacteria, such as V. vulnificus and particular strains of Y. enterocolitica, in the blood
Summary
The virulence of a pathogen is directly related to its capacity to adapt to the environment present within the host, and its ability to escape or subvert the host’s immune response. It is increasingly recognized that together with the other components of the immune response, the host uses a variety of mechanisms and strategies to deprive pathogens of the essential nutrients, such as iron, zinc, and copper [7]. This host response to infection has been coined “nutriprive” or “nutritional immunity” and results from extensive fine-tuning throughout animal evolution [8,9]. Nutritional immunity, and in particular iron deprivation, may be a valuable target in the development of host-directed therapies against infection This development would require a deeper knowledge of the iron metabolic and distribution pathways, which are essential for pathogens and for the host. We will discuss the potential modulation of these pathways to be used as therapeutic targets in the clinics
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