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A more recent version of this article appeared on January 1, 2008

Published online before print October 18, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0707469

Received for publication July 17, 2007.
Revised August 29, 2007.
Accepted for publication September 28, 2007.

Article

Hyperforin down-regulates effector function of activated T lymphocytes and shows efficacy against Th1-triggered CNS inflammatory-demyelinating disease

Anna Cabrelle *{dagger}, Isabella Dell'Aica {ddagger}, Luca Melchiori {ddagger}, Samuela Carraro *{dagger}, Enrico Brunetta *{dagger}, Raffaele Niero *{dagger}, Elisa Scquizzato *{dagger}, Giulia D’Intino {sect}, Laura Calz à{sect}, Spiridione Garbisa {ddagger}@, and Carlo Agostini *{dagger}

*Department of Clinical & Experimental Medicine, Medical School, Padova, Italy; {dagger}Venetian Institute of Molecular Medicine, Padova, Italy; {ddagger}Department of Experimental Biomedical Sciences, Medical School, Padova, Italy; and {sect}DIMORFIPA, Bologna University, Bologna, Italy

@ To whom correspondence should be addressed. E-mail: garbisa{at}unipd.it.


  Abstract

Hyperforin (Hyp) is an active compound contained in the extract of Hypericum perforatum, well known for its antidepressant activity. However, Hyp has been found to possess several other biological properties, including inhibitory effects on tumor invasion, angiogenesis, and inflammation. In this paper, we show that treatment with Hyp inhibited IFN-{gamma} production, with down-regulation of T-box (T-bet; marker of Th1 gene expression) and up-regulation of GATA-3 (marker gene of Th2) on IL-2/PHA-activated T cells. In parallel, we showed a strong down-regulation of the chemokine receptor CXCR3 expression on activated T cells. The latter effect and the down-modulation of matrix metalloproteinase 9 expression may eventually lead to the inhibition of migratory capability and matrix traversal toward the chemoattractant CXCL10 by activated lymphocytes that we observed in vitro. The effect of Hyp was thus evaluated on an animal model of experimental allergic encephalomyelitis (EAE), a classic, Th1-mediated autoimmune disease of the CNS, and we observed that Hyp attenuates the severity of the disease symptoms significantly. Together, these properties qualify Hyp as a putative, therapeutic molecule for the treatment of autoimmune inflammatory disease sustained by Th1 cells, including EAE.

Key Words: inflammation • experimental allergic encephalomyelitis






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Copyright © 2007 by the Society for Leukocyte Biology.