We are analyzing https://link.springer.com/article/10.1186/1742-2094-8-134.

Title:
Toll-like receptors in cerebral ischemic inflammatory injury | Journal of Neuroinflammation
Description:
Cerebral ischemia triggers acute inflammation, which has been associated with an increase in brain damage. The mechanisms that regulate the inflammatory response after cerebral ischemia are multifaceted. An important component of this response is the activation of the innate immune system. However, details of the role of the innate immune system within the complex array of mechanisms in cerebral ischemia remain unclear. There have been recent great strides in our understanding of the innate immune system, particularly in regard to the signaling mechanisms of Toll-like receptors (TLRs), whose primary role is the initial activation of immune cell responses. So far, few studies have examined the role of TLRs in cerebral ischemia. However, work with experimental models of ischemia suggests that TLRs are involved in the enhancement of cell damage following ischemia, and their absence is associated with lower infarct volumes. It may be possible that therapeutic targets could be designed to modulate activities of the innate immune system that would attenuate cerebral brain damage. Ischemic tolerance is a protective mechanism induced by a variety of preconditioning stimuli. Interpreting the molecular mechanism of ischemic tolerance will open investigative avenues into the treatment of cerebral ischemia. In this review, we discuss the critical role of TLRs in mediating cerebral ischemic injury. We also summarize evidence demonstrating that cerebral preconditioning downregulates pro-inflammatory TLR signaling, thus reducing the inflammation that exacerbates ischemic brain injury.
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Keywords {🔍}

tlr, ischemic, pubmed, cerebral, article, brain, ischemia, google, scholar, injury, cas, tlrs, signaling, mice, tolllike, stroke, receptors, role, inflammatory, cells, receptor, response, innate, tolerance, preconditioning, hmgb, damage, central, microglia, immune, activation, cns, tnfα, protein, lps, immunity, neuronal, expression, system, yang, inflammation, cell, myd, irf, model, neuroprotection, focal, cytokines, neurons, pathways,

Topics {✒️}

anti-nucleokine monoclonal antibody high-mobility group box-1 interferon-β promoter-binding protein qing-wu yang nf-κb-induced cytokine tnf-α activate nf-κb-inducing pathways anti-hmgb1 antibody inhibited myd88-independent interferon-beta production tlr4-nf-κb signaling axis o'neill la interferon-beta blocks infiltration article download pdf β-mediated transcription factor β-mediated transcription-factor open access article transcription factors nf-κb interferon-beta administration confers yan-chun wang lipopolysaccharide-induced oligodendrocyte injury post-ischemic brain requires tlr-mediated neuronal damage generates anti-viral molecules prevents tlr4-myd88 interaction numerous anti-inflammatory mediators central nervous system trif-related adaptor molecule receptor-mediated neuronal injury improve neurological behavior ischemia-induced neuronal damage large extra-cellular domain subacute stress-induced neuroinflammation post-ischemic brain tissue ischemia-induced inflammatory injury tlr4-mutant mice subjected ischemia-induced brain damage central immune components preconditioning-induced brain tolerance internal carotid arteries acute cerebral infarction middle cerebral artery high-benefit opportunity important antigen-presenting cells privacy choices/manage cookies smaller infarct size mal/myd88-dependent pathway trif-adaptor independent toll shares common elements marsh bj methylated cytosine-guanosine decrease infarct size

Questions {❓}

Nguyen MD, Julien JP, Rivest S: Innate immunity: the missing link in neuroprotection and neurodegeneration?
Wegener S, Gottschalk B, Jovanovic V, Knab R, Fiebach JB, Schellinger PD, Kucinski T, Jungehulsing GJ, Brunecker P, Muller B, Banasik A, Amberger N, Wernecke KD, Siebler M, Rother J, Villringer A, Weih M: Transient ischemic attacks before ischemic stroke: preconditioning the human brain?
Weih M, Kallenberg K, Bergk A, Dirnagl U, Harms L, Wernecke KD, Einhaupl KM: Attenuated stroke severity after prodromal TIA: a role for ischemic tolerance in the brain?

Schema {🗺️}

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         description:Cerebral ischemia triggers acute inflammation, which has been associated with an increase in brain damage. The mechanisms that regulate the inflammatory response after cerebral ischemia are multifaceted. An important component of this response is the activation of the innate immune system. However, details of the role of the innate immune system within the complex array of mechanisms in cerebral ischemia remain unclear. There have been recent great strides in our understanding of the innate immune system, particularly in regard to the signaling mechanisms of Toll-like receptors (TLRs), whose primary role is the initial activation of immune cell responses. So far, few studies have examined the role of TLRs in cerebral ischemia. However, work with experimental models of ischemia suggests that TLRs are involved in the enhancement of cell damage following ischemia, and their absence is associated with lower infarct volumes. It may be possible that therapeutic targets could be designed to modulate activities of the innate immune system that would attenuate cerebral brain damage. Ischemic tolerance is a protective mechanism induced by a variety of preconditioning stimuli. Interpreting the molecular mechanism of ischemic tolerance will open investigative avenues into the treatment of cerebral ischemia. In this review, we discuss the critical role of TLRs in mediating cerebral ischemic injury. We also summarize evidence demonstrating that cerebral preconditioning downregulates pro-inflammatory TLR signaling, thus reducing the inflammation that exacerbates ischemic brain injury.
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      headline:Toll-like receptors in cerebral ischemic inflammatory injury
      description:Cerebral ischemia triggers acute inflammation, which has been associated with an increase in brain damage. The mechanisms that regulate the inflammatory response after cerebral ischemia are multifaceted. An important component of this response is the activation of the innate immune system. However, details of the role of the innate immune system within the complex array of mechanisms in cerebral ischemia remain unclear. There have been recent great strides in our understanding of the innate immune system, particularly in regard to the signaling mechanisms of Toll-like receptors (TLRs), whose primary role is the initial activation of immune cell responses. So far, few studies have examined the role of TLRs in cerebral ischemia. However, work with experimental models of ischemia suggests that TLRs are involved in the enhancement of cell damage following ischemia, and their absence is associated with lower infarct volumes. It may be possible that therapeutic targets could be designed to modulate activities of the innate immune system that would attenuate cerebral brain damage. Ischemic tolerance is a protective mechanism induced by a variety of preconditioning stimuli. Interpreting the molecular mechanism of ischemic tolerance will open investigative avenues into the treatment of cerebral ischemia. In this review, we discuss the critical role of TLRs in mediating cerebral ischemic injury. We also summarize evidence demonstrating that cerebral preconditioning downregulates pro-inflammatory TLR signaling, thus reducing the inflammation that exacerbates ischemic brain injury.
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