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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

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PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke
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PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke

Published on: June 14, 2018

Post-ischemic inflammation in the brain.

Takashi Shichita1, Ryota Sakaguchi, Mayu Suzuki

  • 1Department of Microbiology and Immunology, School of Medicine, Keio University Tokyo, Japan.

Frontiers in Immunology
|July 27, 2012
PubMed
Summary
This summary is machine-generated.

Post-ischemic inflammation involves immune cells like macrophages and T lymphocytes, crucial for brain injury progression. Understanding these inflammatory mechanisms offers potential for new neuroprotective therapies against stroke.

Keywords:
DAMPsT cellsbraincytokineinflammationischemiamacrophagesstroke

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Post-ischemic inflammation is a key driver of brain ischemia-reperfusion injury.
  • Immune cell infiltration, including macrophages and T lymphocytes, orchestrates this inflammatory response.
  • Toll-like receptors (TLR) 2 and TLR4 mediate inflammation in the sterile ischemic brain environment.

Purpose of the Study:

  • To review the role of infiltrating immune cells in post-ischemic inflammation.
  • To elucidate the mechanisms of immune cell activation and their impact on brain injury.
  • To identify potential therapeutic targets for neuroprotection.

Main Methods:

  • Literature review focusing on immune cell involvement in brain ischemia-reperfusion injury.
  • Analysis of molecular pathways, including Toll-like receptor signaling and cytokine production.
  • Examination of the roles of specific immune cell subsets, such as macrophages and T lymphocytes.

Main Results:

  • Endogenous Toll-like receptor ligands, like high mobility group box 1 (HMGB1), activate macrophages.
  • Activated macrophages release cytokines (e.g., IL-23) that influence T lymphocyte function.
  • Specific T lymphocyte subsets, such as IL-17-producing γδT lymphocytes, exacerbate injury, while regulatory T lymphocytes offer protection.

Conclusions:

  • Infiltrating immune cells, particularly macrophages and T lymphocytes, play a critical role in the inflammatory cascade following brain ischemia.
  • Targeting specific inflammatory pathways and immune cell functions presents a promising strategy for developing novel neuroprotective treatments for stroke.