Yvonne Hagenlocher1, Kristina Kiessling1, Michael Schäffer2, Stephan C Bischoff1, Axel Lorentz3. 1. Department of Nutritional Medicine, University of Hohenheim, Fruwirthstraße 12, 70593, Stuttgart, Germany. 2. Department of General, Visceral, and Thorax Surgery, Marienhospital Stuttgart, Böheimstraße 37, 70199, Stuttgart, Germany. 3. Department of Nutritional Medicine, University of Hohenheim, Fruwirthstraße 12, 70593, Stuttgart, Germany. Lorentz@uni-hohenheim.de.
Abstract
PURPOSE: In terms of their involvement in allergic and inflammatory conditions, mast cells (MC) can be promising targets for medical agents in therapy. Because of their good compliance and effectiveness, phytochemicals are of great interest as new therapeutic tools in form of nutraceuticals. We found recently that cinnamon extract (CE) inhibits mast cell activation. Here, we analysed the effects of a major compound of CE, cinnamaldehyde (CA), on mast cell activation. METHODS: Release of prestored and de novo synthesised mediators as well as expression of pro-inflammatory cytokines and mast cell-specific proteases were analysed in RBL-2H3 cells or in human mast cells isolated from intestinal tissue (hiMC) treated with CA prior to stimulation by FcεRI crosslinking or IONO/PMA. The results were compared with the corresponding effects of CE. RESULTS: Following treatment with CA, release of β-hexosaminidase in IgE-dependent or IgE-independent activated RBL-2H3 cells was down-regulated in a dose-dependent manner to about 10%. In hiMC, release of β-hexosaminidase was also significantly reduced, and release of LTC4 and CXCL8 was almost completely inhibited by CA. Moreover, IgE-mediated expression of CXCL8, CCL2, CCL3 and CCL4 in hiMC was significantly down-regulated by CA. With the exception of the expression of the mast cell proteases tryptase and chymase, the inhibitory effects of CA were very similar to the effects shown for CE treatment. The reducing effect of CA on mast cell mediators-seen for long- and for short-term incubations-could be related to particular signalling pathways as CA caused a down-regulation in ERK as well as PLCγ1 phosphorylation. CONCLUSIONS: CA decreases release and expression of pro-inflammatory mast cell mediators. This inhibitory action is similar to the effects observed for CE indicating CA as the main active compound in CE leading to its anti-allergic properties.
PURPOSE: In terms of their involvement in allergic and inflammatory conditions, mast cells (MC) can be promising targets for medical agents in therapy. Because of their good compliance and effectiveness, phytochemicals are of great interest as new therapeutic tools in form of nutraceuticals. We found recently that cinnamon extract (CE) inhibits mast cell activation. Here, we analysed the effects of a major compound of CE, cinnamaldehyde (CA), on mast cell activation. METHODS: Release of prestored and de novo synthesised mediators as well as expression of pro-inflammatory cytokines and mast cell-specific proteases were analysed in RBL-2H3 cells or in human mast cells isolated from intestinal tissue (hiMC) treated with CA prior to stimulation by FcεRI crosslinking or IONO/PMA. The results were compared with the corresponding effects of CE. RESULTS: Following treatment with CA, release of β-hexosaminidase in IgE-dependent or IgE-independent activated RBL-2H3 cells was down-regulated in a dose-dependent manner to about 10%. In hiMC, release of β-hexosaminidase was also significantly reduced, and release of LTC4 and CXCL8 was almost completely inhibited by CA. Moreover, IgE-mediated expression of CXCL8, CCL2, CCL3 and CCL4 in hiMC was significantly down-regulated by CA. With the exception of the expression of the mast cell proteases tryptase and chymase, the inhibitory effects of CA were very similar to the effects shown for CE treatment. The reducing effect of CA on mast cell mediators-seen for long- and for short-term incubations-could be related to particular signalling pathways as CA caused a down-regulation in ERK as well as PLCγ1 phosphorylation. CONCLUSIONS: CA decreases release and expression of pro-inflammatory mast cell mediators. This inhibitory action is similar to the effects observed for CE indicating CA as the main active compound in CE leading to its anti-allergic properties.
Authors: Matthew J Hamilton; Mark J Sinnamon; Gregory D Lyng; Jonathan N Glickman; Xueli Wang; Wei Xing; Steven A Krilis; Richard S Blumberg; Roberto Adachi; David M Lee; Richard L Stevens Journal: Proc Natl Acad Sci U S A Date: 2010-12-20 Impact factor: 11.205
Authors: Lorina I Badger-Emeka; Promise Madu Emeka; Krishnaraj Thirugnanasambantham; Hairul Islam M Ibrahim Journal: Molecules Date: 2020-11-27 Impact factor: 4.411
Authors: Erika Jensen-Jarolim; Franziska Roth-Walter; Erich Leitner; Stefan Buchleitner; Harald Vogelsang; Tamar Kinaciyan Journal: World Allergy Organ J Date: 2016-01-27 Impact factor: 4.084
Authors: Gerhard J Molderings; Britta Haenisch; Stefan Brettner; Jürgen Homann; Markus Menzen; Franz Ludwig Dumoulin; Jens Panse; Joseph Butterfield; Lawrence B Afrin Journal: Naunyn Schmiedebergs Arch Pharmacol Date: 2016-04-30 Impact factor: 3.000
Authors: Anne Schink; Jan Neumann; Anna Lena Leifke; Kira Ziegler; Janine Fröhlich-Nowoisky; Christoph Cremer; Eckhard Thines; Bettina Weber; Ulrich Pöschl; Detlef Schuppan; Kurt Lucas Journal: PLoS One Date: 2018-10-11 Impact factor: 3.240