Establishing a macrophage model with relevance for oral methacrylate monomer exposures: Attenuated Staphylococcus aureus-induced cytokine release from human macrophages -

Leakage of unpolymerized methacrylate monomers after placement of methacrylate-containing polymeric dental materials leads to human exposure. Based on studies using murine macrophages and LPS from Escherichia coli (E. coli), dental monomers like 2-hydroxyethyl methacrylate (HEMA) are known to inhibit lipopolysaccharide (LPS) induced cytokine release.

The dental monomer hydroxyethyl methacrylate (HEMA) counteracts lipopolysaccharide-induced IL-1β release-Possible role of glutathione. -

HEMA reduced GSH levels and decreased IL-1β release from LPS-stimulated macrophages. The role of GSH in the regulation of IL-1β release was explored. GSH depletion alone could not explain the attenuation of LPS-induced IL-1β release. Electrophile reactivity toward other cellular molecules is a new working hypothesis

Dental monomers inhibit LPS-induced cytokine release from the macrophage cell line RAW264.7 -

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.

Rat lung inflammatory responses after in vivo and in vitro exposure to various stone particles -

Rat lung alveolar macrophages and type 2 cells were exposed for 20 h in vitro to various stone particles with differing contents of metals and minerals (a type of mylonite, gabbro, feldspar, and quartz). The capability to induce the release of the inflammatory cytokines interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), and macrophage inflammatory protein-2 (MIP-2) was investigated.