The DOI matches its Crossref record.
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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Inflammatory mechanisms in ischemic stroke: role of inflammatory cells
Jin, R., Yang, G., & Li, G. (2010) · Journal of Leukocyte Biology · doi:10.1189/jlb.1109766 · Cited by 1,521
“Of the various types of leukocytes, neutrophils are among the first to infiltrate ischemic brain (30 min to a few hours of focal cerebral ischemia), peak earlier (Days 1–3), and then disappear or decrease rapidly with time [8, 23].”
BackgroundInfluentialNeuroinflammation: friend and foe for ischemic stroke
Jayaraj, R. L., Azimullah, S., Beiram, R., Jalal, F. Y., & Rosenberg, G. A. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1516-2 · Cited by 1,479
Pathogenic mechanisms following ischemic stroke
Khoshnam, S. E., Winlow, W., Farzaneh, M., Farbood, Y., & Moghaddam, H. F. (2017) · Neurological Sciences · doi:10.1007/s10072-017-2938-1 · Cited by 636
Post‐ischemic brain damage: pathophysiology and role of inflammatory mediators
Amantea, D., Nappi, G., Bernardi, G., Bagetta, G., & Corasaniti, M. T. (2008) · FEBS Journal · doi:10.1111/j.1742-4658.2008.06766.x · Cited by 473
“21 Lalancette-Hébert M, Gowing G, Simard A, Weng YC & Kriz J (2007) Selective ablation of proliferating”
BackgroundRole of Inflammation and Its Mediators in Acute Ischemic Stroke
Jin, R., Liu, L., Zhang, S., Nanda, A., & Li, G. (2013) · Journal of Cardiovascular Translational Research · doi:10.1007/s12265-013-9508-6 · Cited by 422
“In the subacute phase, infiltrating leukocytes release a variety of proinflammatory mediators including cytokines and chemokines, ROS, MMPs, and other proteases, which further amplify the brain inflammatory responses and cause more extensive activation of brain resident cells and infiltration of blood leukocytes, even…”
Background
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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