title: Dental monomers inhibit LPS-induced cytokine release from the macrophage cell line RAW264.7.
abstract: Methacrylate monomers have been identified in aqueous extracts of freshly cured dental fillings. The hypothesis tested presently was that low concentrations of triethyleneglycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) alone or in combination interfere with the LPS-induced release of cytokines from the macrophage cell line RAW264.7. The cells were exposed to 5-200 μM of monomers for 24 h followed by a 24 h combined exposure to monomers and LPS. TEGDMA reduced LPS-induced release of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), whereas HEMA only reduced IL-1β release. Co-exposure to the two monomers indicated an additive effect. Moreover, the reduced cytokine release persisted for 24 h after termination of the monomer exposure. The LPS-induced activation of proteins in pre-transcriptional signaling pathways (CD14, p-ERK1/2, p-p38, p-JNK, p-IκB-α and p-NFκB-p65) was not altered by monomer exposure, neither were the levels of IL-1β and TNF-α mRNA. However, the LPS-induced level of pro-IL-1β was decreased by the monomer treatment. Thus, HEMA and TEGDMA may interfere with post-transcriptional regulation of synthesis and release of these cytokines. Overall, the results suggest that low concentrations of monomers may cause impaired macrophage responses, and that these effects can persist for up to 24 h after exposure.
authors.affiliation: Nordic Institute of Dental Materials AS, PO Box 3874 Ullevaal stadion, N-0805, Oslo, Norway. Anette.Kocbach@gmail.com
authors.forename: Anette Kocbach
authors.initials: AK
authors.lastname: Bølling
authors.forename: Jan Tore
authors.initials: JT
authors.lastname: Samuelsen
authors.forename: Else
authors.initials: E
authors.lastname: Morisbak
authors.forename: Vibeke
authors.initials: V
authors.lastname: Ansteinsson
authors.forename: Rune
authors.initials: R
authors.lastname: Becher
authors.forename: Jon Einar
authors.initials: JE
authors.lastname: Dahl
authors.forename: Gro Haarklou
authors.initials: GH
authors.lastname: Mathisen
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D053583:Interleukin-1beta / Q000276:immunology* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology* / Q000378:metabolism; D008689:Methacrylates / Q000494:pharmacology*; D051379:Mice; D011092:Polyethylene Glycols / Q000494:pharmacology*; D011109:Polymethacrylic Acids / Q000494:pharmacology*; D012313:RNA / Q000737:chemistry / Q000235:genetics; D012117:Resins, Synthetic / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D008689:Methacrylates; D011109:Polymethacrylic Acids; D012117:Resins, Synthetic; D014409:Tumor Necrosis Factor-alpha; C020946:triethylene glycol dimethacrylate; D011092:Polyethylene Glycols; D012313:RNA; C005044:hydroxyethyl methacrylate