rSj16, a recombinant protein of Schistosoma japonicum-derived molecule, reduces severity of the complete Freund's adjuvant-induced adjuvant arthritis in rats' model

Sj16, a 16-kDa protein produced by Schistosoma japonicum, has been demonstrated to have anti-inflammatory effect. However, the possible mechanism of these phenomena has not been discovered. Here, we tried to touch it with arthritis rats' model induced by injection of complete Freund's adju...

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Veröffentlicht in:Parasite immunology 2010-11, Vol.32 (11-12), p.739-748
Hauptverfasser: SUN, X, LIU, Y.H, LV, Z.Y, YANG, L.L, HU, S.M, ZHENG, H.Q, HU, W, CAO, J.P, FUNG, M.Q, WU, Z.D
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Sprache:eng
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Zusammenfassung:Sj16, a 16-kDa protein produced by Schistosoma japonicum, has been demonstrated to have anti-inflammatory effect. However, the possible mechanism of these phenomena has not been discovered. Here, we tried to touch it with arthritis rats' model induced by injection of complete Freund's adjuvant (CFA). A set of pathogenic characters were observed in CFA-treated rat, including local and systematic read-out, which showed the model successfully set up. After administration of rSj16 (recombinant Sj16) in vivo, paw swelling reduced significantly and in a dose-dependent manner, the level of TNF-α, IL-1β and NO decreased and IL-10 in the serum increased. In vitro, rSj16 reversed the augmented surface expression of CD80, CD86, CD54 and OX6 induced by lipopolysaccharide (LPS) in bone marrow-derived DCs (BMDCs), whereas endocytotic capacity of rSj16-treated dendritic cell (DC) was profoundly increased. IL-12p70 released from rSj16-treated BMDC was decreased but IL-10 increased. Further, following incubation with rSj16 primed BMDCs, the sensitized T cells exhibited increased production of anti-inflammatory IL-10 and IL-4 and decreased production of IL-12p70 and IFN-γ. Collectively, these results implied that rSj16 alleviated CFA-induced arthritis, and the possible mechanisms may be its interruption of maturation and function of DCs. rSj16 could be a potential therapeutic agent against rheumatoid arthritis.
ISSN:0141-9838
1365-3024
DOI:10.1111/j.1365-3024.2010.01240.x