ArticleThe American journal of pathology2006
Gangliosides trigger inflammatory responses via TLR4 in brain glia.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 134 citations in OpenAlex.
- Lysosomes in the immunometabolic reprogramming of immune cells in atherosclerosis.Nature reviews. Cardiology · 2025Review
- Fundamental Neurochemistry Review: Lipids across microglial states.Journal of neurochemistry · 2025Review
- Morphine induces inflammatory responses via both TLR4 and cGAS-STING signaling pathways.Cytokine · 2024Article
- Evaluation of the Choroid Plexus Epithelium Inflammation TLR4/NF-κB/NKCC1 Signal Pathway Activation in the Development of Hydrocephalus.CNS neuroscience & therapeutics · 2024Article
- Molecular Mechanisms in Pathophysiology of Mucopolysaccharidosis and Prospects for Innovative Therapy.International journal of molecular sciences · 2024Review
- Gangliosides and Cell Surface Ganglioside Metabolic Enzymes in the Nervous System.Advances in neurobiology · 2023Article
- Expert-opinion-based guidance for the care of children with lysosomal storage diseases during the COVID-19 pandemic: An experience-based Turkey perspective.Frontiers in public health · 2023Review
- Anti-inflammatory role of GM1 and other gangliosides on microglia.Journal of neuroinflammation · 2022Article
- Sphingolipids, mycobacteria and host: Unraveling the tug of war.Frontiers in immunology · 2022Article
- Sialidase neu4 deficiency is associated with neuroinflammation in mice.Glycoconjugate journal · 2021Article
- Article
- Ganglioside GM1 Targets Astrocytes to Stimulate Cerebral Energy Metabolism.Frontiers in pharmacology · 2021Article
- Phosphoinositides: Roles in the Development of Microglial-Mediated Neuroinflammation and Neurodegeneration.Frontiers in cellular neuroscience · 2021Review
- Hp-s1 Ganglioside Suppresses Proinflammatory Responses by Inhibiting MyD88-Dependent NF-κB and JNK/p38 MAPK Pathways in Lipopolysaccharide-Stimulated Microglial Cells.Marine drugs · 2020Article
- Targeting TLR4-dependent inflammation in post-hemorrhagic brain injury.Expert opinion on therapeutic targets · 2020Review
- Ganglioside Synthesis by Plasma Membrane-Associated Sialyltransferase in Macrophages.International journal of molecular sciences · 2020Article
- Inflammatory mediators of opioid tolerance: Implications for dependency and addiction.Peptides · 2019Review
- Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFOxidative medicine and cellular longevity · 2019Article
- Neuronal and glial factors contributing to sex differences in opioid modulation of pain.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Review
- Therapeutic Strategies Under Development Targeting Inflammatory Mechanisms in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gangliosides participate in various cellular events of the central nervous system and have been closely implicated in many neuronal diseases. However, the precise molecular mechanisms underlying the pathological activity of gangliosides are poorly understood. Here we report that toll-like receptor 4 (TLR4) may mediate the ganglioside-triggered inflammation in glia, brain resident immune cells. Gangliosides rapidly altered the cell surface expression of TLR4 in microglia and astrocytes within 3 hours. Using TLR4-specific siRNA and a dominant-negative TLR4 gene, we clearly demonstrate the functional importance of TLR4 in ganglioside-triggered activation of glia. Inhibition of TLR4 expression by TLR4-siRNA suppressed nuclear factor (NF)-kappaB-binding activity, NF-kappaB-dependent luciferase activity, and transcription of inflammatory cytokines after exposure to gangliosides. Transient transfection of dominant-negative TLR4 also attenuated NF-kappaB-binding activity and interleukin-6 promoter activity. In contrast, these activities were slightly elevated in cells with wild-type TLR4. In addition, CD14 was required for ganglioside-triggered activation of glia, and lipid raft formation may be associated with ganglioside-stimulated signal propagation. Taken together, these results suggest that TLR4 may provide an explanation for the pathological ability of gangliosides to cause inflammatory conditions in the brain.
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