ArticleJournal of immunology (Baltimore, Md. : 1950)2008
TLR2 expression in astrocytes is induced by TNF-alpha- and NF-kappa B-dependent pathways.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 71 citations in OpenAlex.
- Innate immune signaling and functions in astrocytes.Nature immunology · 2026Review
- Oligodendroglia as Active Immunomodulators in Demyelinating Diseases.Neuroscience bulletin · 2026Review
- Ultrasonic repression of TRPA1-dependent astrocyte reactivity confers neuroprotection in models of Lewy body dementia.Translational neurodegeneration · 2026Article
- Signaling roles for astrocytic lipid metabolism in brain function.EMBO reports · 2026Review
- Interplay between Pro-inflammatory Mediators and Oxidative Stressinvolved Recurrent Chronic Heart Failure in Elderly Patients with Coronary Stents.Current medicinal chemistry · 2025Article
- Effect of compound polysaccharide on immunity, antioxidant capacity, gut microbiota, and serum metabolome in kittens.Frontiers in microbiology · 2025Article
- The gut microbiota-astrocyte axis: Implications for type 2 diabetic cognitive dysfunction.CNS neuroscience & therapeutics · 2023Review
- Helicobacter pylori outer membrane vesicles induce astrocyte reactivity through nuclear factor-κappa B activation and cause neuronal damage in vivo in a murine model.Journal of neuroinflammation · 2023Article
- Host immune responses in the central nervous system during fungal infections.Immunological reviews · 2022Review
- Role of astroglial toll-like receptors (TLRs) in central nervous system infections, injury and neurodegenerative diseases.Brain, behavior, and immunity · 2021Review
- Neuropeptide and cytokine regulation of pain in the context of substance use disorders.Neuropharmacology · 2020Review
- IL-1β Induced Cytokine Expression by Spinal Astrocytes Can Play a Role in the Maintenance of Chronic Inflammatory Pain.Frontiers in physiology · 2020Article
- High and Low Molecular Weight Hyaluronic Acid Differentially Influences Oxylipins Synthesis in Course of Neuroinflammation.International journal of molecular sciences · 2019Article
- Engineering Controlled Peritumoral Inflammation to Constrain Brain Tumor Growth.Advanced healthcare materials · 2019Article
- Cell Death Pathways: a Novel Therapeutic Approach for Neuroscientists.Molecular neurobiology · 2018Review
- Regulation of microglial activation in stroke.Acta pharmacologica Sinica · 2017Review
- Insensitivity of astrocytes to interleukin 10 signaling following peripheral immune challenge results in prolonged microglial activation in the aged brain.Neurobiology of aging · 2016Article
- Ligand engagement of Toll-like receptors regulates their expression in cortical microglia and astrocytes.Journal of neuroinflammation · 2015Article
- Naltrexone treatment reverses astrocyte atrophy and immune dysfunction in self-harming macaques.Brain, behavior, and immunity · 2015Article
- The MAPK and PI3K pathways mediate CNTF-induced neuronal survival and process outgrowth in hypothalamic organotypic cultures.Journal of cell communication and signaling · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Astrocytes participate in CNS innate immune responses as evident by their ability to produce a wide array of inflammatory mediators upon exposure to diverse stimuli. Although we have established that astrocytes use TLR2 to signal inflammatory mediator production in response to Staphylococcus aureus, a common etiological agent of CNS infections, the signal transduction pathways triggered by this pathogen and how TLR2 expression is regulated remain undefined. Three disparate inhibitors that block distinct steps in the NF-kappaB pathway, namely SC-514, BAY 11-7082, and caffeic acid phenethyl ester, attenuated NO, TNF-alpha, and CXCL2 release from S. aureus-activated astrocytes. Among these proinflammatory mediators, autocrine/paracrine TNF-alpha was pivotal for augmenting TLR2 expression, since receptor levels were not elevated in astrocytes isolated from TNF-alpha knockout mice upon bacterial exposure. Since TLR2 is critical for signaling astrocytic cytokine production in response to S. aureus, we evaluated the effect of TNF-alpha loss on proinflammatory mediator release. Interestingly, among the molecules assayed, only NO production was significantly attenuated in TNF-alpha knockout astrocytes compared with wild-type cells. Similar results were obtained following LPS treatment, suggesting that TNF-alpha is an important regulator of astrocytic TLR2 expression and NO release in response to diverse microbial stimuli. In addition, NF-kappaB inhibitors attenuated TNF-alpha-induced TLR2 expression in astrocytes. Overall, this study suggests that two important anti-bacterial effector molecules, TLR2 and NO, are regulated, in part, by NF-kappaB-dependent autocrine/paracrine effects of TNF-alpha in astrocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.