Modulation of immune response by head injury

Morganti-Kossmann, Maria Cristina; Satgunaseelan, Laveniya; Bye, Nicole; Kossmann, Thomas

doi:10.1016/j.injury.2007.10.005

Cited by 353 publications

(224 citation statements)

References 105 publications

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“…Inflammation is considered critically important in TBI, 32 with inflammatory processes and chemokine signaling now considered major components of the secondary injury cascade and offering attractive potential targets for pharmaceutical neuroprotection. 33 Classically, the brain is considered as being shielded from the immune system by the blood-brain barrier, giving it an immuno-privileged position within the body.…”

Section: Inflammationmentioning

confidence: 99%

“…Both the infiltrating peripheral immune cells and activated glial cells then increase the production of cytokines, thus promoting neuroinflammation. 32 In addition, this transient alteration in blood-brain barrier function has been shown to contribute to the vasogenic component of cerebral edema after TBI. 37 Because compromised blood-brain barrier function may facilitate the acute inflammatory response after TBI, it may well serve as a target for anti-inflammatory drug development, insofar as agents capable of restoring or maintaining the integrity of the blood-brain barrier could help ameliorate the acute phase of CNS inflammation.…”

Section: Inflammationmentioning

confidence: 99%

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Multifunctional Drugs for Head Injury

2009

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Summary: Traumatic brain injury (TBI) remains one of the leading causes of mortality and morbidity worldwide in individuals under the age of 45 years, and, despite extensive efforts to develop neuroprotective therapies, there has been no successful outcome in any trial of neuroprotection to date. In addition to recognizing that many TBI clinical trials have not been optimally designed to detect potential efficacy, the failures can be attributed largely to the fact that most of the therapies investigated have been targeted toward an individual injury factor. The contemporary view of TBI is that of a very heterogenous type of injury, one that varies widely in etiology, clinical presentation, severity, and pathophysiology. The mechanisms involved in neuronal cell death after TBI involve an interaction of acute and delayed anatomic, molecular, biochemical, and physiological events that are both complex and multifaceted. Accordingly, neuropharmacotherapies need to be targeted at the multiple injury factors that contribute to the secondary injury cascade, and, in so doing, maximize the likelihood of a successful outcome. This review focuses on a number of such multifunctional compounds that have shown considerable success in experimental studies and that show maximum promise for success in clinical trials.

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Section: Inflammationmentioning

confidence: 99%

Section: Inflammationmentioning

confidence: 99%

Multifunctional Drugs for Head Injury

2009

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“…This injury is further classified into focal versus diffuse injury. A secondary brain injury develops in the minutes to months following the original insult, progressively contributing to worsened neurological impairment [153]. Death of resident cells of the central nervous system has traditionally been thought to take place in two phases: an early necrotic and an ongoing, long-term apoptotic phase [154,155].…”

Section: Trauma and The Immune Response From A Clinical Perspectivementioning

confidence: 99%

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

Namas¹,

Ghuma²,

Hermus

et al. 2008

Libyan Journal of Medicine

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Abstract; Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.

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“…TBI is related with continued production and release of the pro-inflammatory cytokines interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α), leading to increased extracellular and cerebrospinal fluid (CSF) levels. [1][2][3] Cytokines are significant mediators of local changes within the central nervous system (CNS) and systemic changes involving immune, metabolic and endocrine responses. [2] They mediate a multitude of different actions, ranging from neuroprotective to neurotoxic effects.…”

Section: Resultsmentioning

confidence: 99%

“…Trauma to the brain results in rupture of the blood-brain barrier, leading to accumulation of leukocytes from the systemic circulation, which themselves trigger an inflammatory response characterized by the invasion of circulating immune cells and release of pro-inflammatory cytokines. [1][2][3] Proinflammatory cytokines are a group of proteins including TNF-α, IL-1 and IL-6, which are the key inflammatory mediators, and have similar biological effects. [3] Leptin may act as an inflammatory cytokine and shares structural similarities with cytokines.…”

Section: Discussionmentioning

confidence: 99%

Correlation between leptin and pro-inflammatory cytokines in cortical contusion injury model

Karaoğlan

Akdemir²,

Çınar³

et al. 2011

Ulus Travma Acil Cerrahi Derg

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AMAÇBu çalışmada, deneysel travmatik beyin hasarı sonrası beyin dokusundaki zaman bağımlı leptin konsantrasyonlarındaki değişiklik ve sitokinlerle olan ilişki değerlen-dirildi. GEREÇ VE YÖNTEMSirküler kranyektomi sonrası 33 adet erkek Wistar-Albino sıçan stereotaksik çembere yerleştirildi ve kortikal kontüz-yon hasarı oluşturuldu. Denekler deformasyon derinliğine göre 3 gruba ayrıldı: 0 mm (Kontrol, n=3), 1,5 mm (Orta hasar, n=15), 2,7 mm (Ciddi hasar, n=15). Hayvanlar hasar sonrası birinci, üçüncü ve beşinci günlerde öldürüldü. BULGULAROrta hasar sonrası ilk gün interlökin 1 beta (IL-1β), interlö-kin 6 (IL-6), tümör nekroz faktör alfa (TNF-α) ve leptin seviyelerinin beyin dokusunda belirgin olarak yükseldiği saptandı. Üçüncü ve beşinci günlerde bu seviyelerin kontrol seviyelerine gerilediği görüldü. Ciddi hasar sonrası birinci gün IL-1β, IL-6, TNF-α seviyeleri korele olarak yüksel-di ve sonrasında kontrol seviyelerine döndü. Buna rağmen leptin seviyeleri birinci ve üçüncü gün azaldı, beşinci gün-de ise kontrol seviyelerine ulaştı. SONUÇCiddi beyin hasarı sonrası erken dönemde leptin salınımı-nın azalması, leptin replasmanının bu olguların tedavisinde önemli rol oynayabileceğini düşündürmektedir.Anahtar Sözcükler: İnterlökin-1β, interlökin-6, Leptin, tümör nekroz faktör-α, travmatik beyin hasarı.

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Modulation of immune response by head injury

Cited by 353 publications

References 105 publications

Multifunctional Drugs for Head Injury

Multifunctional Drugs for Head Injury

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

Correlation between leptin and pro-inflammatory cytokines in cortical contusion injury model

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