Methamphetamine (METH) abuse is associated with "METH mouth", characterized by rampant dental decay and destruction of periodontal bone and soft tissues. In periodontitis, monocyte/macrophages, stimulated by bacterial lipopolysaccharide (LPS), produce interleukin-1beta (IL-1beta), contributing to bone and soft tissue degradation. Effects of METH on monocyte/macrophages and its role in periodontitis are unknown. The objective of this study was to determine METH cytotoxicity and effects on constitutive and LPS-stimulated IL-1beta production in THP-1 human monocytes. METH significantly reduced cell viability, assessed by activity of a mitochondrial enzyme, by 20-40% after 24h, with recovery at longer periods. Brief exposure to METH caused <10% cytotoxicity (measured by an assay that detects membrane damage). LPS from E. coli or the periodontopathogen Fusobacterium nucleatum (F. n.) significantly increased IL-1beta production (measured by ELISA). Despite cytotoxicity of some METH concentrations, METH had no significant effect on constitutive IL-1beta production. However, METH generally increased LPS-stimulated IL-1beta levels, reaching statistical significance at 5x10(-5)M METH ( approximately 50% to >100% increase). The study suggests that METH potentiation of periodontopathogen LPS stimulation of IL-1beta in monocytes could contribute to periodontitis in METH abusers, consistent with other studies suggesting a role for increased IL-1beta in deleterious effects of METH.
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