Transient neuroprotection by minocycline following traumatic brain injury is associated with attenuated microglial activation but no changes in cell apoptosis or neutrophil infiltration

Bye, Nicole; Habgood, Mark D.; Callaway, Jennifer K.; Malakooti, Nakisa; Potter, Ann; Kossmann, Thomas; Morganti-Kossmann, Maria Cristina

doi:10.1016/j.expneurol.2006.10.013

Cited by 231 publications

(196 citation statements)

References 48 publications

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“…[85][86][87] In addition to MCP-1, the concentration of the chemokines MIP-1␣, MIP-2, and KC has been reported to increase following TBI in mouse brain. 4 Together, these results highlight the contribution of chemokines in the development of secondary brain injury mediated by the accumulation of active leukocytes that perpetuate inflammatory and neurotoxic cascades.…”

Section: Monocyte Chemoattractant Proteinmentioning

confidence: 81%

“…26,27 In accordance with these findings, preclinical animal experiments testing immunosuppressive drugs such as minocycline or erythropoietin after TBI attributed the neuroprotective mechanisms of these compounds to the reduction of brain IL-1 synthesis. 4,28,29 …”

Section: Interleukin-1mentioning

confidence: 99%

“…88 Currently, the use of nonsteroidal, anti-inflammatory compounds in TBI models are being investigated, but to date the results obtained are ambiguous. 4 Chronic treatment with ibuprofen improved functional and histopathologic outcome in a mouse model of Alzheimer's disease. [89][90][91] Its use in a TBI model, however, failed to confer neuroprotection.…”

Section: Anti-inflammatory Interventions After Tbimentioning

confidence: 99%

“…When sustained or excessive, however, inflammation is the main cause of numerous neuropathologies. 3 Among the pathological changes of the brain tissue, impairment of the blood-brain barrier (BBB) has been demonstrated in the acute post-traumatic period, allowing the entry of circulating neutrophils, monocytes, and lymphocytes to the injured site, directly affecting neuronal survival and death [4][5][6][7][8] (FIG. 1).…”

Section: Introductionmentioning

confidence: 99%

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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: Monocyte Chemoattractant Proteinmentioning

confidence: 81%

Section: Interleukin-1mentioning

confidence: 99%

Section: Anti-inflammatory Interventions After Tbimentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

2010

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“…Using rodent TBI models, it has been reported that expression of monocyte chemo-attractant protein-1 is enhanced in the brain by 4-h post-injury. 67 However, its diagnostic value for the detection of human TBI has not been examined.…”

Section: Chemokinesmentioning

confidence: 99%