Maintaining the appropriate amount of iron in our bodies is important, too little results in anemia and too much is also toxic to the body. Anemia is a symptom of many different diseases including erythroid protoporphyria and beta-thalassemia.
It is also observed in individuals who suffer from chronic diseases such as autoimmune diseases and cancer when it is known as anemia of inflammation.
The protein HRI has been shown to have a role in anemia in individuals with erythroid protoporphyria and beta-thalassemia and new research using HRI-deficient mice by Jan-Jane Chen and colleagues at Massachusetts Institute of Technology, Cambridge, has now suggested a role for this protein in the anemia of inflammation.
When stimulated with LPS, HRI-deficient mice showed impaired maturation of immune cells known as macrophages and mounted an impaired anti-inflammatory response. This was associated with decreased production of hepcidin, a protein that controls iron levels by inhibiting the absorption of dietary iron from the intestine and the release of iron from senescent red blood cells by macrophages. These data indicate that HRI deficiency attenuates hepcidin expression and suggest a role for HRI in the anemia of inflammation.
TITLE: The function of heme-regulated eIF2-alpha kinase in murine iron homeostasis and macrophage maturation
AUTHOR CONTACT:
Jane-Jane Chen
Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
Phone: (617) 253-9674; Fax: (617) 253-3459