Seminars in Hematology
Volume 46, Issue 4 , Pages 351-357, October 2009

Animal Models of Anemia of Inflammation

  • Seth Rivera

      Affiliations

    • Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, CA
    • Corresponding Author InformationAddress 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
  • ,
  • Tomas Ganz

      Affiliations

    • Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, CA
    • Department of Pathology, David Geffen School of Medicine at the University of California, Los Angeles, CA

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.

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

 The work described in this report was funded in part by NIH NIDDK/NHLBI 1K08DK074284-01.

PII: S0037-1963(09)00100-0

doi:10.1053/j.seminhematol.2009.06.003

Seminars in Hematology
Volume 46, Issue 4 , Pages 351-357, October 2009