"Withholding iron from potential pathogens is a host defense strategy. There is evidence that iron overload per se compromises the ability of phagocytes to kill microorganisms. Several hypotheses exist to explain the association of hemochromatosis with infection.
....
The list of infectious disease agents whose virulence is enhanced by iron continues to increase (
Table 1).
5 These pathogens include bacteria (Gram-negative and Gram-positive), fungi, and viruses.
Table 1.
Organisms whose growth in body fluids, cells, tissues, and intact vertebrate hosts is known to be stimulated by excess iron
Fungi Candida, Cryptococcus, Histoplasma, Paracoccidioides, Rhizopus, Trichosporon,
Aspergillus, Pneumocystis
Protozoa Entamoeba, Leishmania, Naegleria, Plasmodium, Toxoplasma, Trypanosoma
Gram-positive and acid-fast bacteria Bacillus, clostridia, corynebacteria, Erysipelothrix, Listeria,
mycobacteria, staphylococci, streptococci, Gemella
Gram-negative bacteria Acinetobacter, Aeromonas, Alcaligenes, Capnocytophaga, Campylobacter,
Chlamydia, Ehrlichia, Enterobacter, Escherichia, Klebsiella, Legionella, Moraxella,
Neisseria, Pasteurella, Proteus, Pseudomonas, Plesiomonas, Shigella, Vibrio,
Yersinia
Viruses Hepatitis B and C, cytomegalovirus, parvovirus, HIV"
http://www.sciencedirect.com/science/article/pii/S1201971207000811
"The iron-regulatory hormone hepcidin is induced early in infection, causing iron sequestration in macrophages and decreased plasma iron; this is proposed to limit the replication of extracellular microbes, but could also promote infection with macrophage-tropic pathogens. The mechanisms by which hepcidin and hypoferremia modulate host defense, and the spectrum of microbes affected, are poorly understood. Using mouse models, we show that hepcidin was selectively protective against siderophilic extracellular pathogens (
Yersinia enterocolitica O9) by controlling non-transferrin-bound iron (NTBI) rather than iron-transferrin concentration."
http://www.bloodjournal.org/content/early/2017/05/02/blood-2017-03-772715?sso-checked=true
"As alluded to earlier, iron is essential for the survival and growth of almost all organisms.
Furthermore, an important strategy of mammalian antimicrobial defense is based on depriving pathogens of this essential nutrient [
21]. One of the best-studied examples of this strategy is Nramp1, the transporter that pumps iron out of the phagosome [
22,
23]. Numerous experiments in mouse models and in tissue culture have shown that the ability of Nramp1 to lower phagosomal iron concentrations influences the survival and growth of several intracellular pathogens, including
Myocbacterium bovis BCG,
Salmonella typhimurium, and
Leishmania donovani. Polymorphisms in the
NRAMP1 gene have also been linked in some human studies to altered susceptibility to tuberculosis and leprosy [
24]. Based on the idea that there may be additional mechanisms that deprive intracellular pathogens of iron, we initiated investigations some years ago to examine the effects of altered FPN expression on the intracellular growth of
S. typhimurium.
"(iron is pumped out of the cell by the exporter ferroportin (FPN))"
We found that elevation of FPN levels in either HeLa cells or J774 murine macrophages led to a significant inhibition of intracellular
Salmonella growth, whereas hepcidin-induced down-regulation of FPN expression had the opposite effect [
25]. Using
Salmonella strains transformed with iron-regulated transcriptional reporters, we showed that elevated FPN levels were associated with the increased expression of a bacterial gene that is induced by low iron concentrations, suggesting that FPN-mediated iron efflux led ultimately to depletion of the element in the immediate microenvironment of the pathogen. Since these original observations, several other groups have replicated our findings, both with
Salmonella and with several other intracellular bacterial pathogens, including
M. tuberculosis,
Chlamydia psittaci,
C. trachomatis, and
Legionella pneumophila [
26–
28]."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085559/
LPS endotoxins have an inhibitory effect on FPN that produces higher iron intracellular levels in macrophages. This may induce higher persistence of some intramacrophage infectious agents.
"Macrophage iron content is further expanded via an inhibitory effect of IFN-γ and LPS on ferroportin transcription thereby reducing cellular iron egress (
Yang et al., 2002;
Ludwiczek et al., 2003)."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4100575/
"Lipopolysaccharide (LPS) is the major molecular component of the outer membrane of Gram-negative bacteria and serves as a physical barrier providing the bacteria protection from its surroundings."
It may be that gut overgrowth of these Gram negative bacteria, and leaky gut may play a role in persistent intrabacterial infections that some of the CFS/ME patient experiments, by increasing iron levels in Macrophages.
@msf
