ArticleMolecular immunology2020
Methamphetamine alters the TLR4 signaling pathway, NF-κB activation, and pro-inflammatory cytokine production in LPS-challenged NR-9460 microglia-like cells.
Article in Molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Molecular Mechanisms of Hippocampal Synaptic Plasticity Disruption Induced by Chronic Methamphetamine Exposure: A Narrative Review.Cellular and molecular neurobiology · 2026Review
- Stimulant use disorder indicative of increased serum soluble intercellular adhesion molecule-1 concentrations with altered brain reward and interoceptive processing.Brain, behavior, and immunity · 2026Observational
- Selenium and Lycopene Ameliorate Methamphetamine-induced Neurotoxicity in Offspring Rats by Suppressing Oxidative Stress, Neuro-inflammation, and Apoptosis.Biological trace element research · 2026Article
- Microbiome-derived metabolites in substance use disorders: Mechanisms and implications.Annals of the New York Academy of Sciences · 2025Review
- Ibudilast-Mediated Suppression of Neuronal TLR4 in the Prefrontal Cortex Mitigates Methamphetamine-Induced Neuroinflammation and Addictive Behaviours.Addiction biology · 2025Article
- A review on traditional Chinese medicine natural products and acupuncture intervention for Alzheimer's disease based on the neuroinflammatory.Chinese medicine · 2024Review
- Heat-Treated ParaprobioticJournal of microbiology and biotechnology · 2024Article
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- Methamphetamine (MA) use and MA-induced psychosis are associated with increasing aberrations in the compensatory immunoregulatory system, interleukin-1α, and CCL5 levels.Translational psychiatry · 2023Article
- A review on the reciprocal interactions between neuroinflammatory processes and substance use and misuse, with a focus on alcohol misuse.The American journal of drug and alcohol abuse · 2023Review
- Role of Microglia in Psychostimulant Addiction.Current neuropharmacology · 2023Review
- Nanowired Delivery of Curcumin Attenuates Methamphetamine Neurotoxicity and Elevates Levels of Dopamine and Brain-Derived Neurotrophic Factor.Advances in neurobiology · 2023Article
- The Crosstalk Between Neurons and Glia in Methamphetamine-Induced Neuroinflammation.Neurochemical research · 2022Review
- Related Effects of Methamphetamine on the Intestinal BarrierFrontiers in medicine · 2022Review
- Elevation of Pro-inflammatory and Anti-inflammatory Cytokines in Rat Serum after Acute Methamphetamine Treatment and Traumatic Brain Injury.Journal of molecular neuroscience : MN · 2022Article
- Methamphetamine Dysregulation of the Central Nervous System and Peripheral Immunity.The Journal of pharmacology and experimental therapeutics · 2021Review
- Neuroprotective Effects of Anti-high Mobility Group Box-1 Monoclonal Antibody Against Methamphetamine-Induced Dopaminergic Neurotoxicity.Neurotoxicity research · 2021Article
- Methamphetamine facilitates pulmonary and splenic tissue injury and reduces T cell infiltration in C57BL/6 mice after antigenic challenge.Scientific reports · 2021Article
- Acute MDPV Binge Paradigm on Mice Emotional Behavior and Glial Signature.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Methamphetamine Compromises the Adaptive B Cell-Mediated Immunity to Antigenic Challenge in C57BL/6 Mice.Frontiers in toxicology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Methamphetamine (METH) is a major public health and safety problem worldwide. METH is psychostimulant that activates microglia via the toll-like receptor (TLR) 4/MD2 complex, modulating the abundant production of pro-inflammatory cytokines in the central nervous system (CNS). The TLR4/MD2 complex on the surface of microglia recognizes pathogen-associated molecular patterns such as lipopolysaccharide (LPS) resulting in brain tissue inflammation and neuronal damage. Since METH has been associated with microglia-induced neurotoxicity, we hypothesized that METH impairs the expression of TLR4 and activation of NF-κB in NR-9460 microglia-like cells after LPS challenge. We demonstrated that METH decreases the distribution and expression of TLR4 receptors on the surface of microglia-like cells after incubation with endotoxin. Moreover, METH impairs the TLR4/MD2 complex signaling pathways, compromises the activation of NF-κB, and reduces the production of pro-inflammatory mediators in microglia-like cells upon LPS stimulation. Interestingly, microglia-like cells treated with METH and challenged with LPS showed considerable cellular morphological changes including enlarged nuclei and ruffled surface. Our results suggest that METH may have a significant impact on microglial-induced neuroinflammation, neurotoxicity, and the CNS defense against infection. It also highlights the importance of studying the effects of METH on the molecular and cellular components of users' CNS immunity. Finally, animal studies exploring the role of METH on the effectors functions of microglia after antigenic exposure are necessary to understand drug-related inflammation and neural damage in users.
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