Plasma Levels of the Beta Chemokine Regulated Upon Activation, Normal T Cell Expressed, and Secreted (RANTES) Correlate With Severe Brain Injury

Lumpkins, Kimberly; Bochicchio, Grant V.; Zagol, Bradley; Ulloa, Kristian; Simard, J. Marc; Schaub, S; Meyer, W.; Scalea, Thomas M.

doi:10.1097/ta.0b013e318160df9b

Cited by 44 publications

(31 citation statements)

References 12 publications

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“…In neonatal sepsis, CCL5 was significantly decreased. In patients with severe brain injury, high levels of CCL5 were measured in venous blood samples, but the origin of CCL5 production was unclear [42]. Local CCL5 levels in our study were unchanged while systemic levels had a peak at 1 and 4 h after wound closure.…”

Section: Discussionmentioning

confidence: 79%

Local and systemic chemokine patterns in a human musculoskeletal trauma model

et al. 2009

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Section: Discussionmentioning

confidence: 79%

Local and systemic chemokine patterns in a human musculoskeletal trauma model

et al. 2009

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“…21 The β-chemokine RANTES seems to track with radiographic head injury severity on computed tomographic scan. 22 Serum IL-8 and Tumor necrosis factor α (TNF-α) have been associated with elevated ICP; specifically, higher levels seem to correlate with the “dose” (pressure × time) of ICP greater than 20 mm Hg. 23 In a later work, the same investigators observed that these elevations preceded the events of intracranial hypertension and cerebral hypoperfusion, leading them to conclude that these inflammatory markers might be used to predict neurologic deterioration.…”

Section: Peripheral Bloodmentioning

confidence: 99%

Clinical evidence of inflammation driving secondary brain injury

Hinson

Rowell

Schreiber

2015

Journal of Trauma and Acute Care Surgery

156

125

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Background Despite advances in both prevention and treatment, traumatic brain injury (TBI) remains one of the most burdensome diseases; 2% of the US population currently lives with disabilities resulting from TBI. Recent advances in the understanding of inflammation and its impact on the pathophysiology of trauma have increased the interest in inflammation as a possible mediator in TBI outcome. Objectives The goal of this systematic review is to address the question: “What is the evidence in humans that inflammation is linked to secondary brain injury?” As the experimental evidence has been well described elsewhere, this review will focus on the clinical evidence for inflammation as a mechanism of secondary brain injury. Data Sources Medline database (1996-Week 1 June 2014), Pubmed and Google Scholar databases were queried for relevant studies. Study Eligibility Criteria Studies were eligible if participants were adults and/or children who sustained moderate or severe TBI in the acute phase of injury, published in English. Studies published in the last decade (since 2004) were preferentially included. Trials could be observational or interventional in nature. Appraisal and Synthesis Methods To address the quality of the studies retrieved, we applied the Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) criteria to assess the limitations of the included studies. Results Trauma initiates local central nervous system as well as systemic immune activation. Numerous observational studies describe elevation of pro-inflammatory cytokines that are associated with important clinical variables including neurologic outcome and mortality. A small number of clinical trials have included immunomodulating strategies, but no intervention to date has proven effective in improving outcomes after TBI. Limitations Inclusion of studies not initially retrieved by the search terms may have biased our results. Additionally, some reports may have been inadvertently excluded due to use of non-search term key words. Conclusions and Implications of Key Findings Clinical evidence of inflammation causing secondary brain injury in humans is gaining momentum. While inflammation is certainly present, it is not clear from the literature at what juncture inflammation becomes maladaptive, promoting secondary injury rather than facilitating repairand identifying patients with maladaptive inflammation (neuro-inflammation, systemic, or both) after TBI remains elusive. Direct agonism/antagonism represents an exciting target for future study. Level of Evidence Systematic review, level III.

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“…The beta chemokine RANTES (regulated on activation, normal T cell expressed and secreted), which is constitutively expressed by different cells in the brain, is elevated after brain injury. This molecule encourages macrophage migration and activation and may correlate with severity of brain injury [17].…”

Section: Pathophysiologymentioning

confidence: 99%

Eye and visual function in traumatic brain injury

Cockerham¹,

Goodrich²,

Weichel³

et al. 2009

JRRD

142

107

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Abstract-Combat blast is an important cause of traumatic brain injury (TBI) in the Department of Veterans Affairs polytrauma population, whereas common causes of TBI in the civilian sector include motor vehicle accidents and falls. Known visual consequences of civilian TBI include compromised visual acuity, visual fields, and oculomotor function. The visual consequences of TBI related to blast remain largely unknown. Blast injury may include open globe (eye) injury, which is usually detected and managed early in the rehabilitation journey. The incidence, locations, and types of ocular damage in eyes without open globe injury after exposure to powerful blast have not been systematically studied. Initial reports and preliminary data suggest that binocular function, visual fields, and other aspects of visual function may be impaired after blast-related TBI, despite relatively normal visual acuity. Damage to the ocular tissues may occur from blunt trauma without rupture or penetration (closed globe injury). Possible areas for research are development of common taxonomy and assessment tools across services, surgical management, and outcomes for blast-related eye injury; the incidence, locations, and natural history of closed globe injury; binocular and visual function impairment; quality of life in affected servicemembers; pharmacological and visual therapies; and practice patterns for screening, management, and rehabilitation.

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Plasma Levels of the Beta Chemokine Regulated Upon Activation, Normal T Cell Expressed, and Secreted (RANTES) Correlate With Severe Brain Injury

Abstract: RANTES was a significant early marker of severe TBI in critically injured trauma patients, consistent with animal models. Future research on the role of RANTES in the pathogenesis of human TBI is warranted.

Cited by 44 publications

References 12 publications

Local and systemic chemokine patterns in a human musculoskeletal trauma model

Local and systemic chemokine patterns in a human musculoskeletal trauma model

Clinical evidence of inflammation driving secondary brain injury

Eye and visual function in traumatic brain injury

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