Hfe, hemochromatosis, is involved in regulation of intestinal iron absorption. Mice that are homozygous for this targeted mutation are viable, fertile, normal in size and recapitulate human hereditary hemochromatosis. Hereditary hemochromatosis is a genetic disorder of iron hyperabsorption that results in hyperferremia and iron loading in tissues. By 4 weeks of age, homozygotes on the 129S6/SvEvTac background display elevated blood iron levels and up to 2.2-fold higher hepatic nonheme iron than controls. At 10 weeks of age, homozygotes on the 129S6/SvEvTac background have up to 3.3-fold higher hepatic nonheme iron than controls. Iron loading is less severe in homozygotes on the C57BL/6J background. Heterozygotes exhibit some iron loading. Macrophages isolated from homozygotes have impaired TLR4/TRAM/TRIF pathway signalling, with reduced production of TNF-alpha and IL-6. When challenged with Salmonella typhimurium induced enterocolitis, homozygotes exhibit a less severe inflammatory response. Expression of Hamp (hepcidin antimicrobial peptide) is reduced in homozygotes. The Donating Investigator notes that the level of iron loading in mutant animals varies based on the iron content of the diet, breeding strategy, and other factors.

These mice carry a targeted mutation of Hfe, hemochromatosis, exhibit iron loading, and have applications in studies of hereditary hemochromatosis, iron homeostasis and innate immune response.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

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