title: Dimethyl sulphoxide and dimethyl sulphone are potent inhibitors of IL-6 and IL-8 expression in the human chondrocyte cell line C-28/I2.
abstract: OBJECTIVE
  Reactive oxygen species (ROS) are highly diffusable and reactive molecules which modulate gene transcription, particularly of pro-inflammatory cytokines which play a crucial role in the nascency and progression of chronic inflammatory diseases such as rheumatoid arthritis (RA) and osteoarthritis (OA). Since thiols could be potent inhibitors of the production of cytokines, the effects of dimethyl sulphoxide (DMSO) and dimethyl sulphone (DMS) on constitutive and IL-1β-induced IL-6 and IL-8 expression in the human chondrocyte cell line C-28/I2 were evaluated.
  
  
  METHODS
  C-28/I2 cells were incubated for 12h with different concentrations of DMSO or DMS. The secretion of IL-6 and IL-8 was quantified by enzyme-linked immunosorbent assays (ELISAs). The impact of DMSO and DMS on the regulation of p38 and ERK1/2 mitogen-activated protein kinases (MAPKs) was confirmed by Western blot experiments. Furthermore, C-28/I2 cells were stimulated with IL-1β in the absence or presence of DMSO and DMS and IL-6 and IL-8 expression was quantified by ELISAs and quantitative real-time polymerase chain reaction (qRT-PCR).
  
  
  RESULTS
  C-28/I2 cells constitutively expressed large quantities of IL-6 and IL-8. Long-term exposure of cells to DMSO (1%) or DMS (100mM) led to a dramatic downregulation of IL-6 and IL-8 expression which was accompanied by the deactivation of ERK1/2. Both substances also blocked IL-1β-induced IL-6 and IL-8 expression.
  
  
  CONCLUSIONS
  In this study, we demonstrate that both DMSO and DMS represent strong anti-inflammatory properties by blocking constitutive as well as IL-1β-induced IL-6 and IL-8 expression in the human chondrocyte cell line C-28/I2.
authors.affiliation: Ludwig Boltzmann Institute for Rheumatology and Balneology, Kurbadstrasse 14, 1100 Vienna, Austria. burkhard.kloesch@gmx.at
authors.forename: Burkhard
authors.initials: B
authors.lastname: Kloesch
authors.forename: Melissa
authors.initials: M
authors.lastname: Liszt
authors.forename: Johann
authors.initials: J
authors.lastname: Broell
authors.forename: Guenter
authors.initials: G
authors.lastname: Steiner
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D019902:Chondrocytes / Q000187:drug effects* / Q000276:immunology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology*; D004789:Enzyme Activation / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects*; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology; D015850:Interleukin-6 / Q000235:genetics* / Q000276:immunology; D016209:Interleukin-8 / Q000235:genetics* / Q000276:immunology; D019950:Mitogen-Activated Protein Kinase 1 / Q000276:immunology; D048052:Mitogen-Activated Protein Kinase 3 / Q000276:immunology; D010766:Phosphorylation / Q000187:drug effects; D013450:Sulfones / Q000494:pharmacology*; D051996:Transcription Factor RelA / Q000276:immunology; D048051:p38 Mitogen-Activated Protein Kinases / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D013450:Sulfones; D051996:Transcription Factor RelA; C025910:dimethyl sulfone; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases; D004121:Dimethyl Sulfoxide