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Methamphetamine cytotoxicity and effect on LPS-stimulated IL-1beta production by human monocytes
D A Tipton1, Z T Legan, M Kh Dabbous
1Department of Bioscience Research, College of Dentistry, The University of Tennessee Health Science Center, 62 South Dunlap Street, Memphis, TN 38163, USA. dtipton@uthsc.edu
Abstract:
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.
Insights
Methamphetamine (METH) abuse may worsen periodontitis by increasing interleukin-1beta (IL-1beta) production in monocytes stimulated by oral bacteria. This suggests METH impacts immune responses, contributing to dental tissue destruction.
Area of Science:
- Oral biology
- Immunology
- Toxicology
Background:
- Methamphetamine (METH) abuse is linked to severe dental problems, known as "METH mouth."
- Periodontitis involves immune cells like monocytes producing interleukin-1beta (IL-1beta), which degrades oral tissues.
- The specific impact of METH on monocyte function and its role in periodontitis remain unclear.
Purpose of the Study:
- To investigate the cytotoxic effects of METH on human monocytes.
- To determine how METH influences the production of IL-1beta by monocytes, both in their normal state and when stimulated by bacterial components.
Main Methods:
- THP-1 human monocytes were exposed to varying concentrations of METH.
- Cell viability was assessed using mitochondrial enzyme activity and membrane damage assays.
- IL-1beta production was measured via ELISA after stimulation with lipopolysaccharide (LPS) from E. coli or Fusobacterium nucleatum.
Main Results:
- METH exhibited dose-dependent cytotoxicity, reducing cell viability by 20-40% at 24 hours.
- Brief METH exposure showed minimal membrane damage (<10%).
- METH did not significantly alter baseline IL-1beta production but potentiated LPS-stimulated IL-1beta levels, with significant increases observed at 5x10(-5)M METH.
Conclusions:
- METH can be cytotoxic to human monocytes.
- METH enhances IL-1beta production in monocytes stimulated by periodontopathogen-associated LPS.
- This potentiation may contribute to the progression of periodontitis in METH abusers.
