Neuroinflammation, Stroke, Blood-Brain Barrier Dysfunction, and Imaging Modalities.
Eduardo Candelario-JalilRick M DijkhuizenTim MagnusPublished in: Stroke (2022)
Maintaining blood-brain barrier (BBB) integrity is crucial for the homeostasis of the central nervous system. Structurally comprising the BBB, brain endothelial cells interact with pericytes, astrocytes, neurons, microglia, and perivascular macrophages in the neurovascular unit. Brain ischemia unleashes a profound neuroinflammatory response to remove the damaged tissue and prepare the brain for repair. However, the intense neuroinflammation occurring during the acute phase of stroke is associated with BBB breakdown, neuronal injury, and worse neurological outcomes. Here, we critically discuss the role of neuroinflammation in ischemic stroke pathology, focusing on the BBB and the interactions between central nervous system and peripheral immune responses. We highlight inflammation-driven injury mechanisms in stroke, including oxidative stress, increased MMP (matrix metalloproteinase) production, microglial activation, and infiltration of peripheral immune cells into the ischemic tissue. We provide an updated overview of imaging techniques for in vivo detection of BBB permeability, leukocyte infiltration, microglial activation, and upregulation of cell adhesion molecules following ischemic brain injury. We discuss the possibility of clinical implementation of imaging modalities to assess stroke-associated neuroinflammation with the potential to provide image-guided diagnosis and treatment. We summarize the results from several clinical studies evaluating the efficacy of anti-inflammatory interventions in stroke. Although convincing preclinical evidence suggests that neuroinflammation is a promising target for ischemic stroke, thus far, translating these results into the clinical setting has proved difficult. Due to the dual role of inflammation in the progression of ischemic damage, more research is needed to mechanistically understand when the neuroinflammatory response begins the transition from injury to repair. This could have important implications for ischemic stroke treatment by informing time- and context-specific therapeutic interventions.
Keyphrases
- cerebral ischemia
- blood brain barrier
- oxidative stress
- atrial fibrillation
- brain injury
- high resolution
- endothelial cells
- subarachnoid hemorrhage
- immune response
- inflammatory response
- cell adhesion
- lipopolysaccharide induced
- physical activity
- neuropathic pain
- anti inflammatory
- lps induced
- primary care
- healthcare
- cell proliferation
- poor prognosis
- spinal cord injury
- metabolic syndrome
- diabetic rats
- cerebrospinal fluid
- intellectual disability
- autism spectrum disorder
- adipose tissue
- insulin resistance
- white matter
- fluorescence imaging
- functional connectivity
- climate change
- chemotherapy induced
- sensitive detection
- weight loss
- high glucose