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International Journal of Medicinal Mushrooms
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ISSN Imprimir: 1521-9437
ISSN En Línea: 1940-4344

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International Journal of Medicinal Mushrooms

DOI: 10.1615/IntJMedMushr.v13.i3.10
pages 213-225

Medicinal Mushroom Lingzhi or Reishi, Ganoderma lucidum (W.Curt.:Fr.) P. Karst., β-Glucan Induces Toll-like Receptors and Fails to Induce Inflammatory Cytokines in NF-κB Inhibitor-Treated Macrophages

Sainkhuu Batbayar
Department of Life Science, University of Seoul, Seoul, Korea
Mi Jeong Kim
Department of Life Sciences, University of Seoul, Seoul, Korea
Ha Won Kim
Department of Life Sciences, University of Seoul Dongdaemun-gu, Jennong-dong 90, Seoul 130-743, South Korea

SINOPSIS

β-Glucan of medicinal Lingzhi or Reishi mushroom, Ganoderma lucidum (BGG), possesses immunostimulatory and anti-tumor activities. Innate immune cells are activated by the binding of β-glucan to the dectin-1 receptor. The present study investigated the immunostimulating activities of BGG, including binding to dectin-1, secretion of cytokines and reactive oxygen species, and induction of Toll-like receptors (TLRs) in RAW264.7 mouse macrophages. Reverse transcription−polymerase chain reaction and flow cytometry were used for the cytokine and TLR analyses. A mouse inflammation antibody array was used for protein-level cytokine analysis. BGG bound to dectin-1 and induced RAW264.7 cell secretion of several cytokines, including granulocyte colony-stimulating factor, interleukin (IL)-6, regulated upon activation normal T cell expressed and secreted (RANTES), tissue inhibitor of metalloproteinase-1, and tumor necrosis factor-alpha. The secretion of these cytokines was further increased by the addition of lipopolysaccharide (LPS). BGG also induced both nitric oxide and inducible nitric oxide synthase (iNOS). Treatment with an inhibitor of nuclear factor-kappa B (NF-κB) reduced the induction of IL-1, IL-6, and iNOS in a concentration-dependent manner. Expressions of TLR2, TLR4, and TLR6 were increased by BGG treatment, and addition of LPS induced further induction of TLR4 and TLR6. Our result indicates that BGG induces macrophage secretion of inflammatory cytokines, which can be potentiated by the presence of LPS, likely by binding to dectin-1 and TLR-2/6 receptors, which activate NF-κB and prompt the secretion of cytokines.


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