differential effect of high and low molecular weight fucoidans on the severity of collagen-induced arthritis in mice

Fucoidans have been extensively studied for their various biological activities but the exact role of fucoidans on the inflammatory processes associated with arthritic disease has not been studied. The effect of the treatment of high, medium and low molecular weight fucoidans (HMWF, MMWF and LMWF, r...

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Published inPhytotherapy research Vol. 24; no. 9; pp. 1384 - 1391
Main Authors Park, Seung-Beom, Chun, Kwang-Rok, Kim, Jae-Kwan, Suk, Kyungho, Jung, Young-Mi, Lee, Won-Ha
Format Journal Article
LanguageEnglish
Published Chichester, UK John Wiley & Sons, Ltd 01.09.2010
Wiley
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Summary:Fucoidans have been extensively studied for their various biological activities but the exact role of fucoidans on the inflammatory processes associated with arthritic disease has not been studied. The effect of the treatment of high, medium and low molecular weight fucoidans (HMWF, MMWF and LMWF, respectively) on the progression of collagen-induced arthritis (CIA) was tested. A daily oral administration of HMWF enhanced the severity of arthritis, inflammatory responses in the joint cartilage and the levels of collagen-specific antibodies, while LMWF reduced the severity of arthritis and the levels of Th1-dependent collagen-specific IgG₂a. Further in vitro analyses, using macrophage cell lines, revealed that the HMWF induced the expression of various inflammatory mediators, and enhanced the cellular migration of macrophages. These stimulatory effects of fucoidan decreased in fucoidans with lower molecular weights and LMWF did not exhibit any pro-inflammatory effects. Interestingly, the oral administration of HMWF enhanced the production of IFN-γ, one of the Th1 cytokines, in collagen-stimulated spleen cells that had been isolated from CIA mice, while LMWF had the opposite effect. These results indicate that HMWF enhances arthritis through enhancing the inflammatory activation of macrophages while LMWF reduces arthritis through the suppression of Th1-mediated Immune reactions. Copyright © 2010 John Wiley & Sons, Ltd.
Bibliography:http://dx.doi.org/10.1002/ptr.3140
ark:/67375/WNG-80SVZ2PJ-N
ArticleID:PTR3140
istex:3475E10FF7B0A85E12C6B1A689D0FF3034BE6032
ISSN:0951-418X
1099-1573
DOI:10.1002/ptr.3140