AI Article Synopsis
- Hepcidin is the key hormone regulating iron levels in mammals, primarily produced by the liver, and is increased during inflammation, which leads to reduced iron levels (hypoferremia).
- In a study with mice infected by Borrelia burgdorferi, elevated hepcidin levels were linked to decreased serum iron.
- Hepcidin production in response to the bacteria occurs in both the liver and spleen, and is directly stimulated in macrophages through activation of the Toll-like receptor 2, rather than being a secondary effect of cytokine release.
Article Abstract
Hepcidin is the major regulator of systemic iron homeostasis in mammals. Hepcidin is produced mainly by the liver and is increased by inflammation, leading to hypoferremia. We measured serum levels of bioactive hepcidin and its effects on serum iron levels in mice infected with Borrelia burgdorferi. Bioactive hepcidin was elevated in the serum of mice resulting in hypoferremia. Infected mice produced hepcidin in both liver and spleen. Both intact and sonicated B burgdorferi induced hepcidin expression in cultured mouse bone marrrow macrophages. Hepcidin production by cultured macrophages represents a primary transcriptional response stimulated by B burgdorferi and not a secondary consequence of cytokine elaboration. Hepcidin expression induced by B burgdorferi was mediated primarily by activation of Toll-like receptor 2.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738575 | PMC |
| http://dx.doi.org/10.1182/blood-2009-03-209577 | DOI Listing |
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