Anemia of inflammation (AI) is a complex multi-organ response to inflammatory disorders. Because AI can result from many infectious and non-infectious inflammatory diseases, multiple mechanisms may contribute to its pathogenesis, including iron restriction, direct erythropoietic suppression, shortened red blood cell survival, and frank hemolysis. Animal models have been helpful in the study of the mechanisms of AI and its potential treatments, but each model reflects distinct aspects of this heterogeneous syndrome. It is therefore important to study a variety of models of AI. This review focuses on the use of infectious and noninfectious mouse models of inflammation that have been shown to manifest anemia. We review many of the models reported in the literature or developed in our laboratory, and discuss their respective merits and drawbacks.
aDepartment of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, CA
bDepartment of Pathology, David Geffen School of Medicine at the University of California, Los Angeles, CA
Address correspondence to Seth Rivera, MD, PhD, Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, 10833 Le Conte Ave, 37-131 CHS, Los Angeles, CA 90095
The work described in this report was funded in part by NIH NIDDK/NHLBI 1K08DK074284-01.
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