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Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 125643, 11 pages
Dextromethorphan Inhibits Activations and Functions in Dendritic Cells
1Institute of Biomedical Science, National Chung-Hsing University, Taichung 402, Taiwan
2Faculty of Medicine, National Yang-Ming University, Taipei 112, Taiwan
3Division of Allergy, Immunology and Rheumatology, Taichung Veterans General Hospital, Taichung 407, Taiwan
4Laboratory of Toxicology and Pharmacology, National Institutes of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
5Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei 100, Taiwan
6Biomedical Technology and Device Research Laboratories, Industrial Technology Research Institute, Hsinchu 300, Taiwan
7Institute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan
8Division of Chest Medicine, Department of Internal Medicine, Changhua Christian Hospital, Changhua 500, Taiwan
9Department of Respiratory Care, College of Health Sciences, Chang Jung Christian University, Tainan 711, Taiwan
10School of Medicine, Chung Shan Medical University, Taichung 402, Taiwan
11Department of Medical Research and Education, Taichung Veterans General Hospital, Taichung 407, Taiwan
Received 1 February 2013; Accepted 25 March 2013
Academic Editor: Beatrice Gaugler
Copyright © 2013 Der-Yuan Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Supplemental Figure 1: DXM cytotoxicity in DCs.
The result showed that there was no marked difference in the percentage of dead cells in cultures containing 100100 µM DXM or PBS treated controls which suggested that DXM did not have any cytotoxicity in DCs.
Supplemental Figure 2: DXM treatment before or after LPS stimulation impaired TNF-alpha an IL-12 production in mBMDCs.
The result showed that DXM suppressed TNF-alpha and IL-12 expression when it was given before or after LPS stimulation, implying that the anti-inflammatory and immunomodulatory effects of DXM could be used for prevention or treatment purposes.
Supplemental Figure 3: DXM impaired TNF-alpha production in mBMDCs stimulated by various TLR ligands.
We tested whether DXM could modulate the activation of immature DCs by other TLR ligands and applied Pam3CSK4, PolyI:C, flagellin, and CpG ODN ligands for TLR1/TLR2, TLR3, TLR5, and TLR9, respectively. The presence of each substance resulted in the release of the proinflammatory cytokine TNF-alpha. This release was completely inhibited by 50 µM of DXM.
Supplemental Figure 4: DXM did not alter IDO and IL-10 expression in LPS+IFN–γ-treated or untreated mBMDC cells.
A) The result showed that DXM at 50 µM did not induce IDO expression or alter LPS-induced IDO expression. In addition, previous studies reported that IL-10 inhibits effector T-cell responses and may induce Tr1 regulatory T-cell differentiation [52,53]. In this study, B) ELISA indicated that no significant alteration in IL-10 expression was found in DCs treated with or without LPS.