Neuroinflammation and peripheral immunity: Focus on ischemic stroke.

Area of Science:

• Neuroscience
• Immunology
• Pathology

Background:

• Ischemic stroke (IS) initiates a significant inflammatory response within the brain, termed neuroinflammation.
• Neuroinflammation involves both resident brain immune cells and infiltrating peripheral immune cells like neutrophils, macrophages, and T lymphocytes.
• Blood-brain barrier disruption exacerbates inflammatory cell infiltration post-IS, while IS also induces peripheral immunosuppression, increasing infection risk.

Purpose of the Study:

• To review the mechanisms of central neuroinflammation following ischemic stroke.
• To examine the phenomenon of stroke-induced immunosuppression and its clinical implications.
• To provide a comprehensive overview of the interplay between neuroinflammation and peripheral immune changes after IS.

Main Methods:

• This is a review article.
• Literature search and synthesis of existing research on neuroinflammation and immunosuppression post-ischemic stroke.
• Analysis of the impact of IS on both central and peripheral immune systems.

Main Results:

• Ischemic stroke causes significant neuroinflammation mediated by immune cells.
• Stroke leads to a systemic immunosuppressive state, elevating the risk of infections like pneumonia.
• Peripheral organs such as the heart, lungs, spleen, and kidneys can also be damaged by stroke.

Conclusions:

• Ischemic stroke triggers complex inflammatory and immunosuppressive responses affecting the brain and body.
• Understanding these dual effects is crucial for managing stroke patients and preventing secondary complications.
• Further research into mitigating neuroinflammation and immunosuppression could improve stroke outcomes.