کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2183254 | 1550298 | 2010 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Lack of galectin-3 alleviates trypanosomiasis-associated anemia of inflammation Lack of galectin-3 alleviates trypanosomiasis-associated anemia of inflammation](/preview/png/2183254.png)
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.
Journal: Immunobiology - Volume 215, Issues 9–10, September–October 2010, Pages 833–841