Journal of Clinical Immunology Research

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Editorial - Journal of Clinical Immunology Research (2023) Volume 6, Issue 3

Neuroinflammatory Pathways in Stroke: Implications for Neuroimmunology and Recovery

Molly Anthony*

Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Florida, US

Corresponding Author:
Molly Anthony
Department of Neurosurgery and Brain Repair
University of South Florida
Morsani College of Medicine
Florida, US

Received: 04-Jul-2023, Manuscript No. AACIR-23-104169; Editor assigned: 07-Jul-2023, Pre QC No. AACIR-23-104169(PQ); Reviewed: 21-Jul-2023, QC No. AACIR-23-104169; Revised: 23-Jul-2023, Manuscript No. AACIR-23-104169(R); Published: 27-Jul-2023, DOI: 10.35841/aacir-6.3.154

Citation: Anthony M. Neuroinflammatory pathways in stroke: Implications for neuroimmunology and recovery. J Clin Immunol. 2023;6(3):154

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Stroke is a devastating neurological condition characterized by the sudden interruption of blood flow to the brain, leading to neuronal damage and functional impairment. In addition to the initial ischemic injury, accumulating evidence highlights the crucial role of neuroinflammatory processes in the pathogenesis and progression of stroke. Neuroinflammatory pathways in stroke involve a complex interplay between immune cells, cytokines, chemokines, and endothelial dysfunction. This essay aims to explore the neuroinflammatory pathways activated in stroke, including the contribution of resident brain cells and infiltrating immune cells. Understanding these pathways is vital for developing targeted therapeutic strategies to modulate the immune response and mitigate the secondary damage associated with stroke [1].

The early inflammatory response: Following the onset of stroke, a cascade of neuroinflammatory processes is initiated within the ischemic brain tissue. This early inflammatory response involves the activation of resident immune cells, endothelial cells, and the recruitment of peripheral immune cells.

Resident immune cells: Microglia, the resident immune cells of the Central Nervous System (CNS), play a pivotal role in the early inflammatory response to stroke. Upon ischemic insult, microglia become activated and undergo morphological changes, transitioning from a ramified to an amoeboid phenotype. Activated microglia release pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β), Tumor Necrosis Factor-alpha (TNF-α), and Reactive Oxygen Species (ROS), exacerbating the inflammatory environment [2].

Endothelial dysfunction: The disruption of the Blood-Brain Barrier (BBB) following stroke contributes to the infiltration of immune cells into the brain parenchyma. Endothelial cells lining the cerebral vessels undergo activation and upregulate adhesion molecules, such as Intercellular Adhesion Molecule-1 (ICAM-1) and Vascular Cell Adhesion Molecule-1 (VCAM- 1), facilitating the adhesion and transmigration of leukocytes into the brain tissue. BBB breakdown also leads to the extravasation of plasma proteins, which further contribute to the inflammatory response.

Infiltrating immune cells: Peripheral immune cells, including neutrophils and monocytes, are recruited to the ischemic brain tissue following stroke. Chemokines, such as Monocyte Chemoattractant Protein-1 (MCP-1) and C-X-C motif Chemokine Ligand 1 (CXCL1), mediate the migration of these cells towards the site of injury. Neutrophils infiltrate the brain tissue early after stroke onset and release proinflammatory mediators, causing tissue damage. Monocytes differentiate into macrophages within the brain, contributing to phagocytosis of cellular debris and secretion of inflammatory cytokines [3].

Secondary neuroinflammation and resolution: Beyond the acute phase, neuroinflammation in stroke can persist and contribute to secondary damage and delayed recovery. However, neuroinflammatory processes are also involved in the resolution and tissue repair phase following stroke [4].

Astrocyte activation: Astrocytes, the most abundant glial cells in the CNS, respond to stroke-induced injury by undergoing reactive astrogliosis. Activated astrocytes release various cytokines and chemokines, including IL-6, IL-10, and Transforming Growth Factor-beta (TGF-β), which can exert both pro-inflammatory and anti-inflammatory effects. Astrocytes also play a role in scar formation and tissue remodeling.

T lymphocytes: T lymphocytes, specifically CD4+ and CD8+ T cells, infiltrate the ischemic brain tissue and contribute to the neuroinflammatory response in stroke [5].


Neuroinflammatory pathways significantly contribute to the pathophysiology of stroke, impacting both acute brain injury and long-term recovery. Understanding the intricacies of these pathways provides opportunities for developing novel therapeutic interventions that aim to modulate the immune response, reduce inflammation, and promote brain repair after stroke. Further research is needed to elucidate the precise mechanisms underlying neuroinflammation and identify effective therapeutic targets to improve stroke outcomes.


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