Source:http://linkedlifedata.com/resource/pubmed/id/18064431
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2008-11-26
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pubmed:abstractText |
Galectins have recently emerged as central regulators of the immune system. We have previously demonstrated that carbohydrate-dependent binding of galectin-2 induces apoptosis in activated T cells. Here, we investigate the potential therapeutic effect of galectin-2 in experimental colitis. Galectin-2 expression and its binding profile were determined by immunohistochemistry. Acute and chronic colitis was induced by dextran sodium sulfate administration and in a T-cell transfer colitis model. Apoptosis was assessed by TdT-mediated dUTP-biotin nick-end labeling, and cytokine secretion was determined by cytometric bead array. We show that galectin-2 was constitutively expressed mainly in the epithelial compartment of the mouse intestine and bind to lamina propria mononuclear cells. During colitis, galectin-2 expression was reduced, but could be restored to normal levels by immunosuppressive treatment. Galectin-2 treatment induced apoptosis of mucosal T cells and thus ameliorated acute and chronic dextran-sodium-sulfate-induced colitis and in a T-helper-cell 1-driven model of antigen-specific transfer colitis. Furthermore, the pro-inflammatory cytokine release was inhibited by galectin-2 treatment. In preliminary toxicity studies, galectin-2 was well tolerated. Our study provides evidence that galectin-2 induces apoptosis in vivo and ameliorates acute and chronic murine colitis. Furthermore, galectin-2 has no significant toxicity over a broad dose range, suggesting that it may serve as a new therapeutic agent in the treatment of inflammatory bowel disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0946-2716
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pubmed:author |
pubmed-author:BerndtUtaU,
pubmed-author:DaneseSilvioS,
pubmed-author:DankofAnjaA,
pubmed-author:DignassAxel UAU,
pubmed-author:GuzyClaudiaC,
pubmed-author:HolzloehnerPamelaP,
pubmed-author:PaclikDanielaD,
pubmed-author:RosewiczStefanS,
pubmed-author:SturmAndreasA,
pubmed-author:WiedenmannBertramB,
pubmed-author:WittigBianca MBM
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pubmed:issnType |
Print
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pubmed:volume |
86
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1395-406
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pubmed:dateRevised |
2011-7-8
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pubmed:meshHeading |
pubmed-meshheading:18064431-Animals,
pubmed-meshheading:18064431-Apoptosis,
pubmed-meshheading:18064431-Colitis,
pubmed-meshheading:18064431-Colon,
pubmed-meshheading:18064431-Cytokines,
pubmed-meshheading:18064431-Dextran Sulfate,
pubmed-meshheading:18064431-Female,
pubmed-meshheading:18064431-Galectin 2,
pubmed-meshheading:18064431-Gene Expression,
pubmed-meshheading:18064431-Mice,
pubmed-meshheading:18064431-Mucous Membrane,
pubmed-meshheading:18064431-T-Lymphocytes
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pubmed:year |
2008
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pubmed:articleTitle |
Galectin-2 induces apoptosis of lamina propria T lymphocytes and ameliorates acute and chronic experimental colitis in mice.
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pubmed:affiliation |
Medizinische Klinik m.S. Hepatologie und Gastroenterologie, Campus Virchow Klinikum, Charité-Universitätsmedizin, Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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