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Title
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Lack of galectin-3 alleviates trypanosomiasis-associated anemia of inflammation
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Author
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Abstract
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| 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 (Ga13(-/-)) mice. T. brucei infected Ga13-/- 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. (C) 2010 Elsevier GmbH. All rights reserved. |
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Language
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English
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Source (journal)
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Immunobiology. - Stuttgart, 1979, currens
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Publication
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Stuttgart
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2010
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ISSN
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0171-2985
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DOI
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10.1016/J.IMBIO.2010.05.028
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Volume/pages
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215
:9-10
(2010)
, p. 833-841
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ISI
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000281536800022
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Full text (Publisher's DOI)
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