title: Iron status, anemia, and plasma erythropoietin levels in acute and chronic mouse models of colitis.
abstract: BACKGROUND
  Approximately one-half of patients with inflammatory bowel disease (IBD) suffer from anemia, with the most prevalent cause being iron deficiency. Accompanying the anemia are increases in erythropoietin, a plasma protein that can initiate the feedback production of new red blood cells. Anemia also occurs in animal models that are used to investigate the mechanisms of IBD; however, the extent to which iron deficiency produces the anemia in these animal models is unknown. Also unknown in the different animal models of IBD is whether the anemia upregulates the production of erythropoietin or, alternatively, whether a decrease in erythropoietin contributes to the induction of anemia.
  
  
  METHODS
  Two mouse models of colitis were used in this study: (1) acute 6-day ingestion of dextran sodium sulfate and (2) T-cell transfer into lymphopenic recipient mice. Measurements included indices of colitis severity, hematocrit, blood hemoglobin, plasma erythropoietin, serum iron concentration, plasma iron-binding capacities, transferrin saturation, and tissue iron concentrations.
  
  
  RESULTS
  Both models of colitis induced significant decreases in hematocrit, blood hemoglobin, and transferrin saturation, with the spleen and liver showing a decrease in iron content in the T-cell transfer model. Additionally, both models of colitis demonstrated significant increases in plasma erythropoietin and plasma iron-binding capacities.
  
  
  CONCLUSIONS
  The measurements of iron, whether in acute (dextran sodium sulfate) or chronic (T-cell transfer) models of colitis, were generally consistent with iron-deficient anemia, with large increases in erythropoietin indicative of tissue hypoxia. These changes in animal models of colitis are similar to those found in human IBD.
authors.affiliation: Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130, USA.
authors.forename: Patsy R
authors.initials: PR
authors.lastname: Carter
authors.forename: Megan N
authors.initials: MN
authors.lastname: Watts
authors.forename: Melissa
authors.initials: M
authors.lastname: Kosloski-Davidson
authors.forename: Kanchanjunga
authors.initials: K
authors.lastname: Prasai
authors.forename: Matthew B
authors.initials: MB
authors.lastname: Grisham
authors.forename: Norman R
authors.initials: NR
authors.lastname: Harris
mesh_terms: D000208:Acute Disease; D000740:Anemia / Q000209:etiology* / Q000378:metabolism; D000818:Animals; D002908:Chronic Disease; D003092:Colitis / Q000150:complications* / Q000378:metabolism; D016264:Dextran Sulfate / Q000633:toxicity*; D004195:Disease Models, Animal; D004921:Erythropoietin / Q000097:blood*; D018398:Homeodomain Proteins / Q000502:physiology; D006801:Humans; D016753:Interleukin-10 / Q000502:physiology; D007501:Iron / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D013601:T-Lymphocytes / Q000637:transplantation*
chemical_list: D018398:Homeodomain Proteins; C556062:IL10 protein, mouse; D004921:Erythropoietin; C064658:RAG-1 protein; D016753:Interleukin-10; D016264:Dextran Sulfate; D007501:Iron