@article {3413,
	title = {Interferon-gamma limits the availability of iron for intramacrophage Salmonella typhimurium.},
	journal = {Eur J Immunol},
	volume = {38},
	year = {2008},
	month = {07/2008},
	pages = {1923-36},
	abstract = {<p>In stimulating effector functions of mononuclear phagocytes, IFN-gamma is of pivotal importance in host defense against intramacrophage pathogens including salmonellae. As the activity of IFN-gamma is modulated by iron and since a sufficient availability of iron is essential for the growth of pathogens, we investigated the regulatory effects of IFN-gamma on iron homeostasis and immune function in murine macrophages infected with Salmonella typhimurium. In Salmonella-infected phagocytes, IFN-gamma caused a significant reduction of iron uptake via transferrin receptor 1 and resulted in an increased iron efflux caused by an enhanced expression of the iron exporter ferroportin 1. Moreover, the expression of haem oxygenase 1 and of the siderophore-capturing antimicrobial peptide lipocalin 2 was markedly elevated following bacterial invasion, with IFN-gamma exerting a super-inducing effect. This observed regulatory impact of IFN-gamma reduced the intracellular iron pools within infected phagocytes, thus restricting the acquisition of iron by engulfed Salmonella typhimurium while concomitantly promoting NO and TNF-alpha production. Our data suggest that the modulation of crucial pathways of macrophage iron metabolism in response to IFN-gamma concordantly aims at withdrawing iron from intracellular Salmonella and at strengthening macrophage immune response functions. These regulations are thus consistent with the principles of nutritional immunity.</p>},
	keywords = {Acute-Phase Proteins, Animals, Antimicrobial Cationic Peptides, Cation Transport Proteins, Cell Line, Ferritins, Heme Oxygenase (Decyclizing), Hepcidins, Interferon-gamma, Iron, Lipocalins, Macrophages, Mice, Nitric Oxide, Oncogene Proteins, Salmonella typhimurium, Transferrin, Tumor Necrosis Factor-alpha},
	issn = {0014-2980},
	doi = {10.1002/eji.200738056},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/18581323},
	author = {Nairz, Manfred and Fritsche, Gernot and Peter Brunner and Talasz, Heribert and Hantke, Klaus and Weiss, G{\"u}nter}
}
@article {3414,
	title = {Pathways for the regulation of body iron homeostasis in response to experimental iron overload.},
	journal = {J Hepatol},
	volume = {43},
	year = {2005},
	month = {10/2005},
	pages = {711-9},
	abstract = {BACKGROUND/AIMS:
Secondary iron overload is a frequent clinical condition found in association with multiple blood transfusions.
METHODS:
To gain insight into adaptive changes in the expression of iron genes in duodenum, liver and spleen upon experimental iron overload we studied C57BL/6 mice receiving repetitive daily injections of iron-dextran for up to 5 days.
RESULTS:
Iron initially accumulated in spleen macrophages but with subsequent increase in macrophage ferroportin and ferritin expression its content in the spleen decreased while a progressive storage of iron occurred within hepatocytes which was paralleled by a significant increase in hepcidin and hemojuvelin expression. Under these conditions, iron was still absorbed from the duodenal lumen as divalent metal transporter-1 expressions were high, however, most of the absorbed iron was incorporated into duodenal ferritin, while ferroportin expression drastically decreased and iron transfer to the circulation was reduced.
CONCLUSIONS:
Experimental iron overload results in iron accumulation in macrophages and later in hepatocytes. In parallel, the transfer of iron from the gut to the circulation is diminished which may be referred to interference of hepcidin with ferroportin mediated iron export, thus preventing body iron accumulation.},
	keywords = {Animals, Disease Models, Animal, Disease Progression, DNA Primers, Duodenum, Gene Expression Regulation, Hepatocytes, Homeostasis, Iron, Iron Overload, Macrophages, Mice, Mice, Inbred C57BL, Polymerase Chain Reaction, RNA},
	issn = {0168-8278},
	doi = {10.1016/j.jhep.2005.03.030},
	url = {http://www.sciencedirect.com/science/article/pii/S0168827805003168$\#$},
	author = {Theurl, Igor and Ludwiczek, Susanne and Eller, Philipp and Seifert, Markus and Artner, Erika and Peter Brunner and Weiss, G{\"u}nter}
}
