title: Antithetical effects of hemicellulase-treated Agaricus blazei on the maturation of murine bone-marrow-derived dendritic cells.
abstract: We report the effects of hemicellulase-treated Agaricus blazei (ABH) on the maturation of bone-marrow-derived dendritic cells (BMDCs). ABH activated immature BMDCs, inducing up-regulation of surface molecules, such as CD40, CD80 and major histocompatibility complex class I antigens, as well as inducing allogeneic T-cell proliferation and T helper type 1 cell development. However, unlike lipopolysaccharide (LPS), ABH did not stimulate the BMDCs to produce proinflammatory cytokines, such as interleukin-12 (IL-12) p40, tumour necrosis factor-alpha, or IL-1beta. In addition, ABH suppressed LPS-induced DC responses. Pretreatment of DCs with ABH markedly reduced the levels of LPS-induced cytokine secretion, while only slightly decreasing up-regulation of the surface molecules involved in maturation. ABH also had a significant impact on peptidoglycan-induced or CpG oligodeoxynucleotide-induced IL-12p40 production in DCs. The inhibition of LPS-induced responses was not associated with a cytotoxic effect of ABH nor with an anti-inflammatory effect of IL-10. However, ABH decreased NF-kappaB-induced reporter gene expression in LPS-stimulated J774.1 cells. Interestingly, DCs preincubated with ABH and then stimulated with LPS augmented T helper type 1 responses in culture with allogeneic T cells as compared to LPS-stimulated but non-ABH-pretreated DCs. These observations suggest that ABH regulates DC-mediated responses.
authors.affiliation: Department of Alternative Medicine and Bioregulation, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi, Japan. masakika@yamanashi.ac.jp
authors.forename: Masaki
authors.initials: M
authors.lastname: Kawamura
authors.forename: Hirotake
authors.initials: H
authors.lastname: Kasai
authors.forename: Limin
authors.initials: L
authors.lastname: He
authors.forename: Xuewen
authors.initials: X
authors.lastname: Deng
authors.forename: Atsuya
authors.initials: A
authors.lastname: Yamashita
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Terunuma
authors.forename: Isao
authors.initials: I
authors.lastname: Horiuchi
authors.forename: Fuminori
authors.initials: F
authors.lastname: Tanabe
authors.forename: Masahiko
authors.initials: M
authors.lastname: Ito
mesh_terms: D000364:Agaricus / Q000187:drug effects / Q000276:immunology*; D000818:Animals; D000946:Antigens, Fungal / Q000276:immunology*; D000954:Antigens, Surface / Q000378:metabolism; D001854:Bone Marrow Cells / Q000276:immunology; D002454:Cell Differentiation / Q000276:immunology; D002455:Cell Division / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology*; D006026:Glycoside Hydrolases / Q000494:pharmacology; D007108:Immune Tolerance; D008070:Lipopolysaccharides / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism; D010047:Ovalbumin / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D015854:Up-Regulation / Q000276:immunology
chemical_list: D000946:Antigens, Fungal; D000954:Antigens, Surface; D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010047:Ovalbumin; D006026:Glycoside Hydrolases; C023305:hemicellulase
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