title: Brazilian propolis ameliorates trinitrobenzene sulfonic acid-induced colitis in mice by inhibiting Th1 differentiation.
abstract: BACKGROUND
  Propolis is a resinous substance collected by honeybees from leaf buds and cracks in the bark of various plants. We previously demonstrated the inhibitory activity of Brazilian propolis ethanolic extract against the differentiation process of Th17 cells and pathogenesis of collagen-induced arthritis, which is an experimental animal model of rheumatoid arthritis. Th1 cells are also involved in several autoimmune and inflammatory diseases, such as inflammatory bowel disease. In the present study, we demonstrated for the first time that Brazilian propolis significantly inhibited the generation of Th1 cells. Furthermore, we hypothesized that the administration of propolis to a murine model of colitis would suppress Th1 cell differentiation and ultimately ameliorate colitis.
  
  
  METHODS
  CD4 T cells were stimulated under Th1-polarizing conditions (immobilized anti-CD3 and anti-CD28 antibodies with IL-12 plus an anti-IL-4 monoclonal antibody for 5days) with or without the propolis ethanolic extract. Cells were characterized for helper T cell subsets by flow cytometric analysis. Furthermore, we investigated the effects of propolis on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in a mouse model.
  
  
  RESULTS
  Propolis dose-dependently reduced the frequency of IFNγ-producing CD4 T cells under Th1-polarizing conditions. Furthermore, the inhibitory effect of propolis on Th1 differentiation was demonstrated in vivo. The severity of colitis in mice fed propolis was significantly lower than that of mice fed the control diet.
  
  
  CONCLUSIONS
  These findings suggest that the suppressive effect of Brazilian propolis on Th1 differentiation may be useful in controlling unbalanced cytokine networks in autoimmune diseases.
authors.affiliation: Laboratory of Immunology and Microbiology, Faculty of Pharmacy, Chiba Institute of Science, 3 Shiomi-cho, Choshi, Chiba 288-0025, Japan. yokamoto@cis.ac.jp
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Okamoto
authors.forename: Takazumi
authors.initials: T
authors.lastname: Hara
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Ebato
authors.forename: Takashi
authors.initials: T
authors.lastname: Fukui
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Masuzawa
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002454:Cell Differentiation / Q000187:drug effects; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology; D006241:Haptens; D007371:Interferon-gamma / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011429:Propolis / Q000494:pharmacology / Q000627:therapeutic use*; D018417:Th1 Cells / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D000893:Anti-Inflammatory Agents; D006241:Haptens; D007371:Interferon-gamma; D014302:Trinitrobenzenesulfonic Acid; D011429:Propolis