Acute Inflammatory Response in Spinal Cord Following Impact Injury

Carlson, Sonia L.; Parrish, Mark E.; Springer, Joe E.; Doty, Ketah D.; Dossett, Lee

doi:10.1006/exnr.1998.6785

Cited by 447 publications

(340 citation statements)

References 44 publications

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“…Their persistence in inflamed tissue reflects a balance between recruitment and apoptosis (11) . Neutrophils accumulate within hours after spinal cord injury (17)(18)(19) , reaching a peak at 3 days post-injury followed by a second peak several weeks later (11) (Figure 2). …”

Section: Leukocytes Microglia/macrophages and Dendritic Cells As Mementioning

confidence: 99%

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Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Trivedi

Olivas

Noble-Haeusslein

2006

Clinical Neuroscience Research

178

133

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The immune response that accompanies spinal cord injury contributes to both injury and reparative processes. It is this duality that is the focus of this review. Here we consider the complex cellular and molecular immune responses that lead to the infiltration of leukocytes and glial activation, promote oxidative stress and tissue damage, influence wound healing, and subsequently modulate locomotor recovery. Immunomodulatory strategies to improve outcomes are gaining momentum as ongoing research carefully dissects those pathways, which likely mediate cell injury from those, which favor recovery processes. Current therapeutic strategies address divergent approaches including early immunoblockade and vaccination with immune cells to prevent early tissue damage and support a wound-healing environment that favors plasticity. Despite these advances, there remain basic questions regarding how inflammatory cells interact in the injured spinal cord. Such questions likely arise as a result of our limited understanding of immune cell/neural interactions in a dynamic environment that culminates in progressive cell injury, demyelination, and regenerative failure.

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Section: Leukocytes Microglia/macrophages and Dendritic Cells As Mementioning

confidence: 99%

“…They produce TNFagr;, IL-1, reactive free radicals, and nitric oxide (17,34) , each of which can be damaging to the spinal cord, as well as keratan sulfate proteoglycans, which form inhibitory boundaries to extending neurites (35) .…”

Section: Leukocytes Microglia/macrophages and Dendritic Cells As Mementioning

confidence: 99%

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Trivedi

Olivas

Noble-Haeusslein

2006

Clinical Neuroscience Research

178

133

View full text Add to dashboard Cite

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“…45 Thus, neutrophil in¯ux in a SCI has been associated with oxidative damage of surrounding healthy tissue. 46 Activated neutrophils have also been said to contribute to the secondary pathology in SCI by inducing endothelial cell damage and methods of inhibiting neutrophil activation have resulted in reduced intramedullary haemorrhaging and functional improvements in motor performance following compression injury. 47,48 Similarly, interventions which reduce the mononuclear phagocyte population after a SCI can lead to reduced secondary tissue damage.…”

Section: In¯ammatory Responsesmentioning

confidence: 99%

“…47,48 Similarly, interventions which reduce the mononuclear phagocyte population after a SCI can lead to reduced secondary tissue damage. 49,50 Furthermore, Carlson et al 46 found a signi®cant correlation between the amount of tissue damage observed after a contusion injury and the number of macrophages/microglia present, with fewer cells apparent in areas where there was greater intact tissue.…”

Section: In¯ammatory Responsesmentioning

confidence: 99%

Progress in Spinal Cord Research - A refined strategy for the International Spinal Research Trust

2000

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Achieving regeneration in the central nervous system represents one of the greatest intellectual and practical challenges in neurobiology, and yet it is an absolute requirement if spinal cord injury patients are to have any hope of recovery. The mission of the International Spinal Research Trust (ISRT), established in 1980, is to raise money speci®cally for spinal research, with a view to ending the permanence of paralysis caused by spinal cord injury. This review summarises some of the major steps forward made in recent years in understanding the mechanisms involved in spinal cord injury and where these discoveries ®t in with the ISRT's overall objectives. We review approaches aimed at (1) preventing immediate adverse reactions to injury such as neuronal death and scar formation; (2) minimising inhibitory properties of the CNS environment and maximising the growth potential of damaged neurons; (3) understanding axonal guidance systems that will be required for directed outgrowth and functional reconnection; and (4) optimising the function of surviving systems. We also discuss infrastructural' prerequisites for applying knowledge gained through spinal research to the clinical condition, including basic scienti®c issues such as developing representative animal models of spinal cord injury and sensitive quantitative methods for assessing growth and functional restoration. In addition, we point out the importance of communication. The need to share knowledge between research groups is vital for advancing our understanding of injury and repair mechanisms. Equally important is the need for communication between basic scientists and clinicians which will be essential for what is the ultimate goal of the ISRT, the development of relevant treatment strategies that will prove bene®cial to the spinal injured patient. Spinal Cord (2000) 38, 449 ± 472

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“…Activated platelets attach to neutrophils via the release and surface expression of platelet P‐selectin from α ‐granules, which binds to P‐selectin glycoprotein ligand‐1 expressed on neutrophils 4. After CNS injury, a dense neutrophil invasion occurs,5, 6, 7 and selectively abrogating neutrophil infiltration is beneficial in animal models of stroke and experimental autoimmune encephalomyelitis 6, 8. We have shown that mechanisms of neutrophil invasion following an innate immune challenge can be unique to their target tissue, allowing for tissue‐specific anti‐inflammatory interventions 9.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil infiltration to the brain is platelet‐dependent, and is reversed by blockade of platelet GPIbα

et al. 2018

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SummaryNeutrophils are key components of the innate immune response, providing host defence against infection and being recruited to non‐microbial injury sites. Platelets act as a trigger for neutrophil extravasation to inflammatory sites but mechanisms and tissue‐specific aspects of these interactions are currently unclear. Here, we use bacterial endotoxin in mice to trigger an innate inflammatory response in different tissues and measure neutrophil invasion with or without platelet reduction. We show that platelets are essential for neutrophil infiltration to the brain, peritoneum and skin. Neutrophil numbers do not rise above basal levels in the peritoneum and skin and are decreased (~60%) in the brain when platelet numbers are reduced. In contrast neutrophil infiltration in the lung is unaffected by platelet reduction, up‐regulation of CXCL‐1 (2·4‐fold) and CCL5 (1·4‐fold) acting as a compensatory mechanism in platelet‐reduced mice during lung inflammation. In brain inflammation targeting platelet receptor GPIbα results in a significant decrease (44%) in platelet‐mediated neutrophil invasion, while maintaining platelet numbers in the circulation. These results suggest that therapeutic blockade of platelet GPIbα could limit the harmful effects of excessive inflammation while minimizing haemorrhagic complications of platelet reduction in the brain. The data also demonstrate the ability to target damaging brain inflammation in stroke and related disorders without compromising lung immunity and hence risk of pneumonia, a major complication post stroke. In summary, our data reveal an important role for platelets in neutrophil infiltration to various tissues, including the brain, and so implicate platelets as a key, targetable component of cerebrovascular inflammatory disease or injury.

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Acute Inflammatory Response in Spinal Cord Following Impact Injury

Cited by 447 publications

References 44 publications

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Inflammation and spinal cord injury: Infiltrating leukocytes as determinants of injury and repair processes

Progress in Spinal Cord Research - A refined strategy for the International Spinal Research Trust

Neutrophil infiltration to the brain is platelet‐dependent, and is reversed by blockade of platelet GPIbα

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