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Inflammation in Ischemic Brain Injury: Timing Is Important
Abstract
Inflammation is a defense reaction against diverse insults that serves to remove noxious agents and to limit their detrimental effects. There is increasing evidence that post-ischemic inflammation plays an important role in brain ischemia. However, whether inflammatory processes are deleterious or beneficial to recovery is presently a matter of debate and controversy. Experimentally and clinically, stroke is followed by an acute and a prolonged inflammatory response characterized by the production of inflammatory cytokines, leukocyte and monocyte infiltration in the brain, and the activation of resident glial cells. These events may contribute to ischemic brain injury. Several groups report conflicting results regarding the role of inflammation and effects of anti-inflammatory treatments in cerebral ischemia. Experimental studies employing knockout mice for different cytokines and chemokines provide only partial answers. This highlights the importance of clarifying the role of the immune response in pathological changes at the site of ischemic lesions in the brain. Here, we describe dual effects of the brain's inflammatory response and new evidence for a neuroprotective role of proliferating microglial cells in ischemia. In addition, we discuss a potential role of post-ischemic inflammation in brain regeneration and modulation of synaptic plasticity.
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“Resident macrophages and invading myelomonocytic cells release cytokines (such as TNFα and IL-1β), chemokines, reactive oxygen species (ROS), neutrophil extracellular traps (NETs), and MMP-9, which lead to further disruption of the BBB, brain edema, neuronal death, and hemorrhagic transformation (Fig. 4) (136).”
From The anatomy and immunology of vasculature in the central nervous system (2019) · cites this paper as [136]
In the citing paper
“The acute phase after ischemia is characterized by the rapid-release DAMPs, which are sensed by endothelial cells as well as resident and circulating immune cells.”
From The anatomy and immunology of vasculature in the central nervous system (2019) · cites this paper as [136]
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Items 201–238 of 238
Molecular Pathways of Ischemic Stroke and Advanced Therapeutic Strategies
Singh, P. (2018) · International Journal of Science Technology & Society · doi:10.18091/ijsts.4122 · Cited by 1
“The post ischemic condition in brain is characterized by inflammation with different changes, such as microglial cells rapid activation and infiltration of circulating inflammatory cells as demonstrated in animal models as well as stroke patients (Jin et al., 2010; Kriz, 2006; Xia et al., 2010).”
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“There is a growing body of evidence that post-ischemic inflammation plays a vital role in mediating the downstream effects of brain ischemia (3).”
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“Penumbra is estimated to remain viable for 16 to 48 hours after stroke, allowing possible clinical actions (Candelario-Jalil, 2009; Dirnagl et al., 1999; Durukan and Tatlisumak, 2007; Kadhim et al., 2008; Kriz, 2006; Lakhan et al., 2009; Meisel et al., 2005).”
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“Stroke followed by infiltration of leukocytes, release cytokines and chemokines and reactive oxygen species which amplify the brain-inflammatory response, eventually leading to disruption of the BBB, cerebral edema, neuronal death, and hemorrhagic transformation (Kriz, 2006; Amantea et al., 2009).”
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Modelling of ischemic stroke : focus on co-morbidities and therapeutic intervention
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Pathophysiology of Stroke: A Molecular Mechanism Perspective
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Metadata
- Authors
- Kriz, J.
- Venue
- Critical Reviews™ in Neurobiology
- Publisher
- Begell House
- Published
- 2006
- Volume
- 18
- Issue
- 1-2
- Pages
- 145-157
- ISSN
- 0892-0915 (ISSN-L)
- OpenAlex
- W1982308497
- Cited by
- 238
- References
- 0
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 13 · 2023: 12 · 2022: 11 · 2021: 8 · 2020: 7 · 2019: 21 · 2018: 10 · 2017: 8 · 2016: 13 · 2015: 13 · 2014: 21 · 2013: 23 · 2012: 18
- FWCI
- 3.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Critical Reviews in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- post-ischemic inflammation, cerebral ischemia, stroke, neuroinflammation, inflammatory cytokines, leukocyte infiltration, monocyte infiltration, glial activation, microglia, neuroprotection, anti-inflammatory therapy, cytokine knockout mice, brain regeneration, synaptic plasticity
- MeSH terms
- Animals, Brain Ischemia, Chemotaxis, Leukocyte, Encephalitis, Gliosis, Humans, Cytokines, Microglia, Cytoprotection, Brain Infarction, Cell Proliferation
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