title: Feeding administration of Daikenchuto suppresses colitis induced by naive CD4+ T cell transfer into SCID mice.
abstract: OBJECTIVE
  Daikenchuto, a traditional Japanese herbal medicine, suppresses bacterial translocation by improvement of gastrointestinal motility and blood flow. As Daikenchuto reportedly reduces gastrointestinal inflammatory activity by these mechanisms, we analyzed whether Daikenchuto suppresses experimental colitis and reduces inflammatory cytokine expression in a mouse model.
  
  
  METHODS
  Colitis was induced by transfer of naive CD4(+) T cells of BALB/c mice into SCID mice, and mice were given either control or 2.7 % Daikenchuto-containing feed. We investigated body weight, clinical symptoms, histological changes, and Th1- and Th17-cytokine expression. Cytokine mRNA expression was analyzed using real-time RT-PCR. The ratio of IL-17(+) and IFN-γ(+) CD4(+) T cells were analyzed by flow cytometry.
  
  
  RESULTS
  Daikenchuto delayed the development of colitis and significantly reduced the histological inflammation scores. Analyses of cytokine mRNA revealed that Th17 cytokines were significantly decreased in colons of mice that received Daikenchuto. Absolute numbers of IL-17(+) or IFN-γ(+) CD4(+) T cells per colon were less in mice receiving Daikenchuto than in mice that received control feed, as both groups received naive CD4(+) T cells to induce colitis.
  
  
  CONCLUSIONS
  We demonstrated that feeding administration of Daikenchuto suppresses colitis induced by naive CD4(+) T cell transfer into SCID mice. Daikenchuto may show clinical benefit in the treatment of human inflammatory bowel disease and further studies are warranted.
authors.affiliation: Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. tiwasa@intmed3.med.kyushu-u.ac.jp
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Iwasa
authors.forename: Haruei
authors.initials: H
authors.lastname: Ogino
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nakamura
authors.forename: Eikichi
authors.initials: E
authors.lastname: Ihara
authors.forename: Hirotada
authors.initials: H
authors.lastname: Akiho
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Takayanagi
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000502:physiology*; D003092:Colitis / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D003106:Colon / Q000378:metabolism / Q000473:pathology; D015536:Down-Regulation; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology; D007564:Japan; D008518:Medicine, East Asian Traditional; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D005894:Panax; D010936:Plant Extracts / Q000008:administration & dosage*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013047:Specific Pathogen-Free Organisms; D018417:Th1 Cells / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology; D013997:Time Factors; D032106:Zanthoxylum; D030521:Zingiberaceae
chemical_list: D020381:Interleukin-17; D010936:Plant Extracts; D012333:RNA, Messenger; C121414:dai-kenchu-to; D007371:Interferon-gamma