Epigallocatechin-3-gallate, constituent of green tea, suppresses the LPS-induced phenotypic and functional maturation of murine dendritic cells through inhibition of mitogen-activated protein kinases and NF-κB

Ahn, Soon‐Cheol; Kim, Gi‐Young; Kim, Jinhyung; Baik, Seong-Wan; Han, Myung‐Kwan; Lee, Hee-Jeong; Moon, Dong‐Oh; Lee, Chang-Min; Kang, Ju-Hyung; Kim, Bo-Hye; Oh, Yang-Hyo; Park, Yeong‐Min

doi:10.1016/j.bbrc.2003.11.108

Cited by 92 publications

(59 citation statements)

References 46 publications

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“…15,42 In a co-culture study, 42 separately treating either APCs (during the antigen ovalbumin pulse) or T cells (ovalbumin specific) with EGCG-reduced T-cell proliferation, however, the direct effect of EGCG on T cells was predominant. Together with the previous studies showing that in vitro supplementation of EGCG suppressed maturation of mouse bone marrow-derived 43 and human monocyte-derived 44 dendritic cells, we believe that, although T cells are the main target of EGCG effect, contribution of APCs to EGCGinduced inhibition of autoreactive T-cell proliferation should be considered. More directed, definitive work is needed to accurately elucidate this question.…”

Section: Discussionsupporting

confidence: 63%

Epigallocatechin-3-Gallate Ameliorates Experimental Autoimmune Encephalomyelitis by Altering Balance among CD4+ T-Cell Subsets

Wang

Ren

et al. 2012

The American Journal of Pathology

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The green tea component epigallocatechin-3-gallate (EGCG) may be beneficial in autoimmune diseases; however, the underlying mechanisms are not well understood. In this study, we determined the effect of EGCG on the development of experimental autoimmune encephalomyelitis, an animal model for human multiple sclerosis, and the underlying mechanisms. Female C57BL/6 mice were fed EGCG (0%, 0.15%, 0.3%, and 0.6% in diet) for 30 days and then immunized with specific antigen myelin oligodendrocyte glycoprotein 35-55. EGCG dose dependently attenuated clinical symptoms and pathological features (leukocyte infiltration and demyelination) in the central nervous system and inhibited antigen-specific T-cell proliferation and delayed-type hypersensitivity skin response. We further showed that EGCG reduced production of interferon-␥, IL-17, IL-6, IL-1␤, and tumor necrosis factor-␣; decreased types 1 and 17 helper T cells (Th1 and Th17, respectively); and increased regulatory T-cell populations in lymph nodes, the spleen, and the central nervous system. Moreover, EGCG inhibited expression of transcription factors T-box expressed in T cells and retinoid-related orphan receptor-␥t, the specific transcription factor for Th1 and Th17 differentiation, respectively; the plasma levels of intercellular adhesion molecule 1; and CCR6 expression in CD4 ؉ T cells. These results indicate that EGCG may attenuate experimental autoimmune encephalomyelitis autoimmune response by inhibiting immune cell infiltration and modulating the balance among pro-and anti-autoimmune CD4 ؉ T-cell subsets.Thus, we identified a novel mechanism that underlies EGCG's beneficial effect in autoimmune disease. (Am J

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Section: Discussionsupporting

confidence: 63%

Epigallocatechin-3-Gallate Ameliorates Experimental Autoimmune Encephalomyelitis by Altering Balance among CD4+ T-Cell Subsets

Wang

Ren

et al. 2012

The American Journal of Pathology

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“…Inhibition of the tyrosine kinase activities of growth factor receptors such as epidermal growth factor receptor, platelet-derived growth factor receptor, and fibroblast growth factor receptor has been observed for EGCG with an IC 50 of 1-2 M in A431 human epidermoid carcinoma cells (40). Several studies show that EGCG at higher concentrations (5-100 M) also perturbs downstream signaling, repressing the mitogen-activated protein kinase pathway, activator protein-1, and nuclear factor-B (41)(42)(43)(44)(45)(46)(47)(48), although other studies have indicated EGCG increased mitogen-activated protein kinase and activator protein-1 activity (37,49). Decreases in nitric oxide production by EGCG was observed, apparently caused by reduction of inducible nitric oxide synthase gene expression at concentrations of 1-10 M (50).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Inhibition of Tumor Angiogenesis and Vascular Tumor Growth by Epigallocatechin-3-Gallate

Fassina

Venè

Morini

et al. 2004

Clinical Cancer Research

170

109

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Purpose: Green tea consumption has been linked to a reduced occurrence of some tumor types. Current data indicate that the principal mediator of this chemopreventive effect is epigallocatechin-3-gallate (EGCG), the most abundant polyphenol found in dried tea leaves. Here, we examined the effects of this compound on the two key cell populations typically involved in tumor growth: tumor cells and endothelial cells.Experimental Design: The effects of green tea and EGCG were tested in a highly vascular Kaposi's sarcoma (KS) tumor model and on endothelial cells in a panel of in vivo and in vitro assays.Results: EGCG inhibited KS-IMM cell growth and endothelial cell growth, chemotaxis, and invasion over a range of doses; high concentrations also induced tumor cell apoptosis. EGCG inhibited the metalloprotease-mediated gelatinolytic activity produced by endothelial cell supernatants and the formation of new capillary-like structures in vitro. Green tea or purified EGCG when administered to mice in the drinking water inhibited angiogenesis in vivo in the Matrigel sponge model and restrained KS tumor growth. Histological analysis of the tumors were consistent with an anti-angiogenic activity of EGCG and green tea. Conclusions:These data suggest that the green tea gallate or its derivatives may find use in the prevention and treatment of vascular tumors in a chemoprevention or adjuvant setting.

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“…Thus, MAPKs are important targets for anti-inflammatory activity. Previous studies demonstrated the suppressive effect of high doses of EGCG on the LPS-induced MAPK pathway, but the influence of physiologically relevant levels of EGCG is entirely unknown (34). Therefore, we examined whether 1 mM EGCG suppresses LPS-induced MAPK activation through 67LR (Fig.…”

Section: Effect Of 67lr Downregulation On Egcg-induced Inactivation Omentioning

confidence: 99%

TLR4 Signaling Inhibitory Pathway Induced by Green Tea Polyphenol Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor

Byun¹,

Fujimura

Yamada³

et al. 2010

The Journal of Immunology

152

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Epigallocatechin-3-gallate, constituent of green tea, suppresses the LPS-induced phenotypic and functional maturation of murine dendritic cells through inhibition of mitogen-activated protein kinases and NF-κB

Cited by 92 publications

References 46 publications

Epigallocatechin-3-Gallate Ameliorates Experimental Autoimmune Encephalomyelitis by Altering Balance among CD4+ T-Cell Subsets

Epigallocatechin-3-Gallate Ameliorates Experimental Autoimmune Encephalomyelitis by Altering Balance among CD4+ T-Cell Subsets

Mechanisms of Inhibition of Tumor Angiogenesis and Vascular Tumor Growth by Epigallocatechin-3-Gallate

TLR4 Signaling Inhibitory Pathway Induced by Green Tea Polyphenol Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor

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