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We are analyzing https://link.springer.com/article/10.1186/1742-2094-8-89.

Title:
Poly(I:C) promotes TNFα/TNFR1-dependent oligodendrocyte death in mixed glial cultures | Journal of Neuroinflammation
Description:
Background Activation of glial cells via toll-like receptors (TLRs) and other intracellular pathogen recognition receptors promotes the release of potentially toxic acute phase reactants such as TNFα and nitric oxide into the extracellular space. As such, prolonged glial activation, as is thought to occur during a persistent viral infection of the CNS, may contribute to both neurodegeneration and demyelination. However, the effects of virus-induced glial activation on oligodendrocytes are not fully understood. Method To determine the effects of glial activation on oligodendrocyte viability we treated primary glial cultures isolated from neonatal rats or mice with the RNA viral mimic poly(I:C) and in some cases other TLR ligands. TLR3 expression was determined by western blot. Cytokine levels were measured by RT-PCR, ELISA, and intracellular cytokine staining. Oligodendrocyte precursor (preOL) viability was determined by Alamar blue assays and immunocytochemistry. Result Stimulation of mixed glial cultures with poly(I:C) resulted in microglia activation, TNFα production and preOL toxicity. This toxic effect of poly(I:C) was indirect as it failed to affect preOL viability in pure cultures despite the fact that preOLs express TLR3. Poly(I:C)-induced loss of preOLs was abolished in TNFα or TNFR1 deficient mixed glial cultures, suggesting that TNFα/TNFR1 signaling is required for poly(I:C) toxicity. Furthermore, although both microglia and astrocytes express functional TLR3, only microglia produced TNFα in culture. Consistent with these findings, other TLR agonists similarly triggered TNFα production and preOL toxicity in mixed glial cultures. Conclusion Activation of microglia by poly(I:C) promotes TNFα/TNFR1-dependent oligodendroglial cell death. These data indicate that during an ongoing viral infection of the CNS, microglial TNFα may be detrimental to oligodendrocytes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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  • Science
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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We can't see how the site brings in money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

tnfα, polyic, pubmed, cultures, article, google, scholar, microglia, glial, astrocytes, mixed, tlr, cas, cells, stimulation, figure, lps, preol, production, viability, activation, oligodendrocyte, μgml, cell, glia, results, tnfr, central, experiments, death, oligodendrocytes, preols, ccl, infection, cns, treated, multiple, viral, demyelination, determined, toxicity, pbs, data, expression, sclerosis, treatment, stimulated, independent, receptor, receptors,

Topics {✒️}

tlr2-myd88/mal-dependent inflammatory responses anti-tumor necrosis factor double-stranded rna viruses sds-polyacrylamide gel electrophoresis retinoic acid-inducible gene lipopolysaccharide-induced oligodendrocyte injury article download pdf inflammation-induced secondary injury pre-oligodendrocyte cell death virus-induced glial activation poly-d-lysine coated 6 tumor necrosis factor central nervous system double-stranded rna triggered tnf-mediated toxicity tnfα-mediated oligodendrocyte toxicity placebo-controlled multicenter study intraspinal microglial/macrophage activation direct cell-cell contact mediates rantes/ccl5 expression tumour necrosis factor virus-induced encephalitis tnfα/tnfr1-dependent mechanism glial inflammatory responses full size image tlr agonists tested adaptive immune responses antiviral immune responses related subjects lps-induced preol cytotoxicity oligodendrocyte progenitor cells promotes preol cytotoxicity oligodendroglial cell death research grant rg3975 privacy choices/manage cookies steelman & jianrong li inducing oligodendrocyte death gram-negative bacteria authors’ original file adaptive immune requirements mixed neuronal cultures induce cell death induced preol death de bakker pi de las heras vesicular stomatitis virus lymphocytic choriomeningitis virus microglial responses result inflammatory demyelinating events rna viral infection

Questions {❓}

  • Galea I, Bechmann I, Perry VH: What is immune privilege (not)?
  • Munz C, Lunemann JD, Getts MT, Miller SD: Antiviral immune responses: triggers of or triggered by autoimmunity?
  • Williams A, Piaton G, Lubetzki C: Astrocytes--friends or foes in multiple sclerosis?

Schema {🗺️}

WebPage:
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         headline:Poly(I:C) promotes TNFα/TNFR1-dependent oligodendrocyte death in mixed glial cultures
         description:Activation of glial cells via toll-like receptors (TLRs) and other intracellular pathogen recognition receptors promotes the release of potentially toxic acute phase reactants such as TNFα and nitric oxide into the extracellular space. As such, prolonged glial activation, as is thought to occur during a persistent viral infection of the CNS, may contribute to both neurodegeneration and demyelination. However, the effects of virus-induced glial activation on oligodendrocytes are not fully understood. To determine the effects of glial activation on oligodendrocyte viability we treated primary glial cultures isolated from neonatal rats or mice with the RNA viral mimic poly(I:C) and in some cases other TLR ligands. TLR3 expression was determined by western blot. Cytokine levels were measured by RT-PCR, ELISA, and intracellular cytokine staining. Oligodendrocyte precursor (preOL) viability was determined by Alamar blue assays and immunocytochemistry. Stimulation of mixed glial cultures with poly(I:C) resulted in microglia activation, TNFα production and preOL toxicity. This toxic effect of poly(I:C) was indirect as it failed to affect preOL viability in pure cultures despite the fact that preOLs express TLR3. Poly(I:C)-induced loss of preOLs was abolished in TNFα or TNFR1 deficient mixed glial cultures, suggesting that TNFα/TNFR1 signaling is required for poly(I:C) toxicity. Furthermore, although both microglia and astrocytes express functional TLR3, only microglia produced TNFα in culture. Consistent with these findings, other TLR agonists similarly triggered TNFα production and preOL toxicity in mixed glial cultures. Activation of microglia by poly(I:C) promotes TNFα/TNFR1-dependent oligodendroglial cell death. These data indicate that during an ongoing viral infection of the CNS, microglial TNFα may be detrimental to oligodendrocytes.
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      headline:Poly(I:C) promotes TNFα/TNFR1-dependent oligodendrocyte death in mixed glial cultures
      description:Activation of glial cells via toll-like receptors (TLRs) and other intracellular pathogen recognition receptors promotes the release of potentially toxic acute phase reactants such as TNFα and nitric oxide into the extracellular space. As such, prolonged glial activation, as is thought to occur during a persistent viral infection of the CNS, may contribute to both neurodegeneration and demyelination. However, the effects of virus-induced glial activation on oligodendrocytes are not fully understood. To determine the effects of glial activation on oligodendrocyte viability we treated primary glial cultures isolated from neonatal rats or mice with the RNA viral mimic poly(I:C) and in some cases other TLR ligands. TLR3 expression was determined by western blot. Cytokine levels were measured by RT-PCR, ELISA, and intracellular cytokine staining. Oligodendrocyte precursor (preOL) viability was determined by Alamar blue assays and immunocytochemistry. Stimulation of mixed glial cultures with poly(I:C) resulted in microglia activation, TNFα production and preOL toxicity. This toxic effect of poly(I:C) was indirect as it failed to affect preOL viability in pure cultures despite the fact that preOLs express TLR3. Poly(I:C)-induced loss of preOLs was abolished in TNFα or TNFR1 deficient mixed glial cultures, suggesting that TNFα/TNFR1 signaling is required for poly(I:C) toxicity. Furthermore, although both microglia and astrocytes express functional TLR3, only microglia produced TNFα in culture. Consistent with these findings, other TLR agonists similarly triggered TNFα production and preOL toxicity in mixed glial cultures. Activation of microglia by poly(I:C) promotes TNFα/TNFR1-dependent oligodendroglial cell death. These data indicate that during an ongoing viral infection of the CNS, microglial TNFα may be detrimental to oligodendrocytes.
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