title: Cinnamon extract inhibits degranulation and de novo synthesis of inflammatory mediators in mast cells.
abstract: BACKGROUND
  Mast cells (MC) are main effector cells of allergic and other inflammatory reactions; however, only a few anti-MC agents are available for therapy. It has been reported that cinnamon extract (CE) attenuates allergic symptoms by affecting immune cells; however, its influence on MC was not studied so far. Here, we analyzed the effects of CE on human and rodent MC in vitro and in vivo.
  
  
  METHODS
  Expression of MC-specific proteases was examined in vivo in duodenum of mice following oral administration of CE. Release of mediators and phosphorylation of signaling molecules were analyzed in vitro in human MC isolated from intestinal tissue (hiMC) or RBL-2H3 cells challenged with CE prior to stimulation by FcεRI cross-linking.
  
  
  RESULTS
  Following oral treatment with CE, expression of the mast cell proteases MCP6 and MC-CPA was significantly decreased in mice. In hiMC, CE also caused a reduced expression of tryptase. Moreover, in hiMC stimulated by IgE cross-linking, the release of β-hexosaminidase was reduced to about 20% by CE. The de novo synthesis of cysteinyl leukotrienes, TNFα, CXCL8, CCL2, CCL3, and CCL4, was almost completely inhibited by CE. The attenuation of mast cell mediators by CE seems to be related to particular signaling pathways, because we found that activation of the MAP kinases ERK, JNK, and p38 as well as of Akt was strongly reduced by CE.
  
  
  CONCLUSIONS
  CE decreases expression of mast cell-specific mediators in vitro and in vivo and thus is a new plant-originated candidate for anti-allergic therapy.
authors: Department of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
authors: Y
authors: Y
authors: Hagenlocher
authors: I
authors: I
authors: Bergheim
authors: S
authors: S
authors: Zacheja
authors: M
authors: M
authors: Schäffer
authors: S C
authors: SC
authors: Bischoff
authors: A
authors: A
authors: Lorentz
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015550:Cell Degranulation / Q000187:drug effects* / Q000276:immunology; D002460:Cell Line; D002478:Cells, Cultured; D002935:Cinnamomum zeylanicum / Q000737:chemistry*; D016207:Cytokines / Q000096:biosynthesis; D004386:Duodenum / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors; D006801:Humans; D007155:Immunologic Factors / Q000008:administration & dosage / Q000494:pharmacology; D018836:Inflammation Mediators / Q000378:metabolism*; D016209:Interleukin-8 / Q000096:biosynthesis; D015289:Leukotrienes / Q000096:biosynthesis; D008407:Mast Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D010447:Peptide Hydrolases / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D010936:Plant Extracts / Q000008:administration & dosage / Q000494:pharmacology*; D017455:Receptors, IgE / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D053802:Tryptases / Q000378:metabolism
chemical_list: D016207:Cytokines; D007155:Immunologic Factors; D018836:Inflammation Mediators; D016209:Interleukin-8; D015289:Leukotrienes; D010936:Plant Extracts; D017455:Receptors, IgE; D048049:Extracellular Signal-Regulated MAP Kinases; D010447:Peptide Hydrolases; D053802:Tryptases