title: The water-soluble extract from cultured medium of Ganoderma lucidum (Reishi) mycelia (Designated as MAK) ameliorates murine colitis induced by trinitrobenzene sulphonic acid.
abstract: Ganoderma lucidum Karst is well known as 'Reishi', a traditional food in China and Japan. It contains a polysaccharide component known to induce granulocyte macrophage colony-stimulating factor (GM-CSF) production from murine splenocytes. Moreover, GM-CSF may be a therapeutic agent for Crohn's disease. In this study, we investigated the water-soluble, polysaccharide components of Reishi (designated as MAK) in murine colitis induced by trinitrobenzene sulphonic acid (TNBS). We examined the concentration of GM-CSF in peritoneal macrophage cells (PMs) of C57BL/6 mice during in vitro and in vivo stimulation with MAK. After feeding with chow or MAK for 2 weeks, 2 mg of TNBS/50% ethanol was administered to each mouse. After 3 days of TNBS treatment, intestinal inflammation was evaluated, and mononuclear cells of the mesenteric lymph nodes (MLNs) and colon were cultured for ELISA. To determine the preventive role of GM-CSF, the mice were pre-treated with or without anti-GM-CSF antibody before TNBS administration. In vitro and in vivo MAK-stimulated PMs produced GM-CSF in a dose-dependent manner. Intestinal inflammation by TNBS was improved by feeding with MAK. MLNs of mice treated with TNBS produced IFN-γ, which was inhibited by feeding with MAK. In contrast, MLNs of mice treated with TNBS inhibited GM-CSF production, which was induced by feeding with MAK. The colon organ culture assay also revealed that IFN-γ was decreased and GM-CSF was increased by MAK. The preventive effect was blocked by the neutralization of GM-CSF. We concluded that the induction of GM-CSF by MAK may provide the anti-inflammatory effect.
authors.affiliation: Department of Medicine and Molecular Science, Hiroshima University, Hiroshima, Japan             Department of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Hanaoka
authors.forename: Y
authors.initials: Y
authors.lastname: Ueno
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Nagai
authors.forename: T
authors.initials: T
authors.lastname: Onitake
authors.forename: K
authors.initials: K
authors.lastname: Yoshioka
authors.forename: K
authors.initials: K
authors.lastname: Chayama
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D000911:Antibodies, Monoclonal / Q000008:administration & dosage; D002478:Cells, Cultured; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D003106:Colon / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D003470:Culture Media / Q000378:metabolism; D004195:Disease Models, Animal; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D017737:Macrophages, Peritoneal / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D025282:Mycelium / Q000254:growth & development / Q000378:metabolism*; D020940:Reishi / Q000276:immunology*; D014302:Trinitrobenzenesulfonic Acid / Q000008:administration & dosage
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D003470:Culture Media; D004365:Drugs, Chinese Herbal; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D014302:Trinitrobenzenesulfonic Acid