Involvement of inflammatory cytokines in central nervous system injury

Wang, Chen Xu; Shuaib, Ashfaq

doi:10.1016/s0301-0082(02)00010-2

Cited by 230 publications

(173 citation statements)

References 128 publications

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“…11,16 Besides their involvement in immune processes, cytokines also func- tion as mediators of intracellular communication 17 and play a pivotal role in tissue homeostasis of the mature organism.…”

Section: Cytokines and Chemokines Produced In The Injured Brainmentioning

confidence: 99%

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

2010

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Summary:Despite dramatic improvements in the management of traumatic brain injury (TBI), to date there is no effective treatment available to patients, and morbidity and mortality remain high. The damage to the brain occurs in two phases, the initial primary phase being the injury itself, which is irreversible and amenable only to preventive measures to minimize the extent of damage, followed by an ongoing secondary phase, which begins at the time of injury and continues in the ensuing days to weeks. This delayed phase leads to a variety of physiological, cellular, and molecular responses aimed at restoring the homeostasis of the damaged tissue, which, if not controlled, will lead to secondary insults. The development of secondary brain injury represents a window of opportunity in which pharmaceutical compounds with neuroprotective properties could be administered. To establish effective treatments for TBI victims, it is imperative that the complex molecular cascades contributing to secondary injury be fully elucidated. One pathway known to be activated in response to TBI is cellular and humoral inflammation. Neuroinflammation within the injured brain has long been considered to intensify the damage sustained following TBI. However, the accumulated findings from years of clinical and experimental research support the notion that the action of inflammation may differ in the acute and delayed phase after TBI, and that maintaining limited inflammation is essential for repair. This review addresses the role of several cytokines and chemokines following focal and diffuse TBI, as well as the controversies around the use of therapeutic anti-inflammatory treatments versus genetic deletion of cytokine expression.

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Section: Cytokines and Chemokines Produced In The Injured Brainmentioning

confidence: 99%

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

2010

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“…These findings show for the first time that an inflammatory mediator that is central to a variety of vascular diseases induces vasodilation through Ca 2ϩ spark activation. TNF-␣ is produced in the brain during ischemia and is implicated in the etiology of several cardiovascular diseases, including stroke, cardiac failure, coronary artery disease, and atherosclerosis (15,46). TNF-␣ is reported to induce both vasoconstriction and vasodilation.…”

Section: Discussionmentioning

confidence: 99%

“…cerebrovascular circulation; ryanodine-sensitive Ca 2ϩ release channel; Ca 2ϩ -activated K ϩ channel; reactive oxygen species; vasodilation STROKE AND TRANSIENT BRAIN ISCHEMIA are vasculature-borne brain pathologies accompanied by inflammatory changes in blood vessels and parenchymal tissues (15,46). TNF-␣, a pleiotropic cytokine, is a proinflammatory agent generated by glial cells, neurons, macrophages, and vascular endothelium during brain injury.…”

mentioning

confidence: 99%

“…TNF-␣, a pleiotropic cytokine, is a proinflammatory agent generated by glial cells, neurons, macrophages, and vascular endothelium during brain injury. Clinical data demonstrate a correlation between TNF-␣ levels and the severity of ischemic brain damage, but controversy exists regarding the functional role of TNF-␣, with both beneficial and detrimental roles having been proposed (3,8,9,15,36,46). Chronic TNF-␣ elevation is associated with risk factors for other vascular pathologies, including coronary artery disease and atherosclerosis (26).…”

mentioning

confidence: 99%

“…During stroke, TNF-␣ may cause neuronal damage directly and by accelerating ischemia-induced local inflammatory responses. In contrast, studies also indicate that TNF-␣ may be cytoprotective (8,15,36,46). TNF-␣ acts in a paracrine manner by binding to two membrane receptors, p55 and p75.…”

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confidence: 99%

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TNF-α dilates cerebral arteries via NAD(P)H oxidase-dependent Ca²⁺ spark activation

Cheranov

Jaggar²

2006

American Journal of Physiology-Cell Physiology

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Caspase‐1–processed interleukins in hyperoxia‐induced cell death in the developing brain

Felderhoff‐Mueser

Sifringer

Polley

et al. 2004

Annals of Neurology

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Infants born prematurely may develop neurocognitive deficits without an obvious cause. Oxygen, which is widely used in neonatal medicine, constitutes one possible contributing neurotoxic factor, because it can trigger neuronal apoptosis in the developing brain of rodents. We hypothesized that two caspase-1-processed cytokines, interleukin (IL)-1␤ and IL-18, are involved in oxygen-induced neuronal cell death. Six-day-old Wistar rats or C57/BL6 mice were exposed to 80% oxygen for various time periods (2, 6, 12, 24, and 48 hours). Neuronal cell death in the brain, as assessed by Fluoro-Jade B and silver staining, peaked at 12 to 24 hours and was preceded by a marked increase in mRNA and protein levels of caspase 1, IL-1␤, IL-18, and IL-18 receptor ␣ (IL-18R␣). Intraperitoneal injection of recombinant human IL-18 -binding protein, a specific inhibitor of IL-18, attenuated hyperoxic brain injury. Mice deficient in IL-1 receptor-associated kinase 4 (IRAK-4), which is pivotal for both IL-1␤ and IL-18 signal transduction, were protected against oxygen-mediated neurotoxicity. These findings causally link IL-1␤ and IL-18 to hyperoxia-induced cell death in the immature brain. These cytokines might serve as useful targets for therapeutic approaches aimed at preserving neuronal function in the immature brain, which is exquisitely sensitive to a variety of iatrogenic measures including oxygen. Neurol 2005;57:50 -59 Advances in the understanding of fetal physiology have resulted in markedly increased survival rates of premature infants. Ann

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Involvement of inflammatory cytokines in central nervous system injury

Cited by 230 publications

References 128 publications

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

TNF-α dilates cerebral arteries via NAD(P)H oxidase-dependent Ca²⁺ spark activation

Caspase‐1–processed interleukins in hyperoxia‐induced cell death in the developing brain

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Involvement of inflammatory cytokines in central nervous system injury

Cited by 230 publications

References 128 publications

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

TNF-α dilates cerebral arteries via NAD(P)H oxidase-dependent Ca2+ spark activation

Caspase‐1–processed interleukins in hyperoxia‐induced cell death in the developing brain

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TNF-α dilates cerebral arteries via NAD(P)H oxidase-dependent Ca²⁺ spark activation