Lack of galectin-3 alleviates trypanosomiasis-associated anemia of inflammation

Vankrunkelsven Ann, De Ceulaer Kris, Hsu Daniel, Fu-Tong Liu, De Baetselier Patrick, Stijlemans Benoît

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


A typical pathological feature associated with experimental African trypanosomiasis (Trypanosoma brucei infection in mice) is anemia of chronic disease (ACD), which is due to a sustained type 1 cytokine-mediated inflammation and hyperactivation of M1 macrophages. Galectin-3 (Gal-3) was amply documented to contribute to the onset and persistence of type 1 inflammatory responses and we herein document that this protein is strongly upregulated during T. brucei infection. We evaluated the involvement of Gal-3 in trypanosomiasis-associated anemia using galectin-3 deficient (Gal3-/-) mice. T. brucei infected Gal3-/- mice manifested significant lower levels of anemia during infection and survived twice as long as wild type mice. Moreover, such mice showed increased levels of serum IL-10 and reduced liver pathology (as evidenced by lower AST/ALT levels). In addition, there was also an increase in gene expression of iron export genes and a reduced expression of genes, which are associated with accumulation of cellular iron.Our data indicate that Gal-3 is involved in the development of inflammation-associated anemia during African trypanosomiasis, possibly due to a disturbed iron metabolism that in turn may also lead to liver malfunction.

Original languageEnglish (US)
Pages (from-to)833-841
Number of pages9
Issue number9-10
StatePublished - Sep 2010


  • African trypanosomiasis
  • Anemia of chronic disease
  • Erythrophagocytosis
  • Galectin-3
  • Inflammation
  • Iron homeostasis
  • Liver pathology

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Hematology


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