Differential Release of Interleukines 6, 8, and 10 in Cerebrospinal Fluid and Plasma After Traumatic Brain Injury

Maier, Bernd Oliver; Schwerdtfeger, Karsten; Mautes, A.; Holanda, M.; Müller, Martin; Steudel, W. I.; Marzi, Ingo

doi:10.1097/00024382-200115060-00002

Cited by 121 publications

(76 citation statements)

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“…#significant difference (p < 0.05) between "TBI" and "MT + TBI". cytokine levels in TBI patients cannot be simply the brain itself, as alterations of the blood-brain barrier did not influence the distribution pattern of cytokines in CSF and serum after trauma [21].…”

Section: Discussionmentioning

confidence: 97%

Serum IL-6, IL-8 and IL-10 Levels in Multiple Trauma Compared to Traumatic Brain Injury and Combined Trauma

Seekamp

Griensven

Lehmann

et al. 2002

European Journal of Trauma

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Background: In recent studies, the role of cytokines in traumatic brain injury (TBI) has been identified and the intrathecal origin of cytokines demonstrated. The question, however, whether or not there is any difference in serum cytokines between TBI, multiple trauma (MT) and the combination of both (MT with TBI) which may significantly contribute to the final outcome, has not been fully examined yet. Patients and Methods: In a prospective study three different groups of trauma patients were monitored for serum cytokine levels over a 7-day period, multiple organ dysfunction (MOD) and final outcome. The patients eligible for this study must have sustained either an isolated traumatic brain injury (TBI), or multiple trauma (MT) without TBI, or a multiple trauma in combination with TBI (MT+TBI). Results: In patients with isolated TBI (n = 40, cranial Abbreviated Injury Score [AIS head ] = 4.4 ± 0.8, total Injury Severity Score [ISS] = 17.1 ± 5.1), serum interleukin-(IL-)6 levels ranged between 150 and 200 pg/ml within the first 48 h followed by a constant decline (< 100 pg/ml) over the 7-day study period. By contrast, serum IL-6 levels of multiply injured patients (n = 10, AIS head = 1.0 ± 1.2, total ISS = 29.9 ± 5.2) were significantly (p < 0.05) increased (range 350-400 pg/ml) after trauma, also followed by a constant decline. In patients suffering from MT including TBI (n = 44, AIS head = 4.1 ± 0.9, total ISS = 31.8 ± 5.8), serum IL-6 levels were also significantly (p < 0.05) higher after trauma compared to TBI patients, but not significantly different from MT patients without TBI. IL-8 and IL-10 serum levels demonstrated a similar pattern, with low cytokine serum levels in the TBI group but significantly high serum levels in both MT groups. The multiple organ dysfunction (MOD) score of Marshall et al revealed no significant change in the TBI group over the 7-day period. In MT patients the MOD score deteriorated transiently around day 3, whereas in the combined trauma group the MOD score was elevated over the entire study period compared to both other trauma groups. Mortality was 27.5% in TBI patients, 0 in MT, and 52.3% in combined trauma. Conclusion: TBI alone does not result in a significant systemic inflammatory response, whereas the combination of TBI and MT seems to enhance the inflammatory reaction ending in a higher MOD incidence and MOD-related mortality as compared to MT without TBI.

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Section: Discussionmentioning

confidence: 97%

Serum IL-6, IL-8 and IL-10 Levels in Multiple Trauma Compared to Traumatic Brain Injury and Combined Trauma

Seekamp

Griensven

Lehmann

et al. 2002

European Journal of Trauma

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“…An increase in the level of interleukin (IL) 8, IL-6, IL-10 and peripheral monocytes count after intracranial hemorrhage and traumatic brain injury shows the effect of these inflammatory mediators in the degeneration process and secondary insult. These mediators also have effect on multiple organ dysfunctions after severe brain injury (5,11,13,14). In addition to these inflammatory degenerative factors, increased release of growth factors, neurotrophins and anti-inflammatory mediators including transforming growth factor β1 (TGF β1) and IL-10 protects the neurons against the excitotoxicities, acidosis, hypoxia and peroxidants after acute brain injuries (12).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of tgf β1, il-8 and nitric oxide in the serum of diffuse axonal injury patients and its association with clinical status and outcome

Sohrevardi¹,

Ahmadinejad²,

Said³

et al. 2012

Turkish Neurosurgery

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AIm:The aim was to evaluate the level of interleukin 8 (IL-8), transforming growth factor β1 (TGF β1) and Nitric oxide (NO) in diffuse axonal injury (DAI) and its association to the outcome and clinical status. mAterIAl and methOds: This cross-sectional study was conducted on 20 patients with DAI and 20 patients with multiple traumas without head injury and 20 healthy subjects as controls. Blood levels of IL-8, TGF β1 and nitric oxide in the 1st, 2nd, 3rd and 7th days of injury were measured. Glasgow coma scale (GCS) of patients was recorded. The patients' outcome was evaluated by Glasgow Outcome Scale (GOS). results:The level of TGF β1 was increasing during the admission and had the maximum level at the 7th day. In the DAI group, there was significant correlation between GOS score and serum IL-8 at 7th day of admission (r=-0.68, p= 0.002). In this group the GCS was found to be significantly correlated with the IL-8 concentration at 7th day of admission (p= 0.026, r=-0.55).COnClusIOn: IL-8 has negative correlation with GCS and GOS. TGF β1 could protect the brain from cytotoxics, hypoxia and acidosis so its level comes down in brain injuries as a result of its overuse. BulGulAr: TGF β1 düzeyi hastaneye yatışla birlikte artıyordu ve maksimum düzeye 7. günde ulaştı. DAY grubunda GOS skoru ile yattıktan sonraki 7. gün serum IL-8 değeri arasında anlamlı bir korelasyon vardı (r=-0,68, p= 0,002). Bu grupta GCS'nin yattıktan sonra 7. günde IL-8 konsantrasyonuyla önemli ölçüde korelasyon gösterdiği bulundu (p= 0,026, r=-0,55).sOnuÇ: IL-8'in GCS ve GOS ile negatif korelasyonu vardır. TGF β1 beyni sitotoksik maddeler, hipoksi ve asidozdan koruyabilir ve bu nedenle beyin yaralanmalarında fazla kullanılmasıyla düzeyi düşer.

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“…The involvement of neuroinflammation in both acute neuropathological conditions, such as stroke or brain trauma, and chronic neurodegenerative disorders, such as Alzheimer's or Parkinson's diseases, has been well described in the literature (Akiyama et al, 2000;Boutin et al, 2001;Cicchetti et al, 2002;Hirsch et al, 2005;Jander and Stoll, 1998;Jander et al, 2002;Koistinaho and Koistinaho, 2005;Lindberg et al, 2005;Maier et al, 2001;Ouchi et al, 2005;Perini et al, 2001;Pinteaux et al, 2006;Rothwell et al, 1997;Stoll et al, 1998;Tuppo and Arias, 2005;Yu and Lau, 2000). The relationship between neuroinflammation and neurodegeneration is strong but complex, as shown by observations that neuroinflammation may be either detrimental or beneficial following neuronal injury (Ali et al, 2000;Boutin et al, 2001;Grilli et al, 2000;Ooboshi et al, 2005;Pinteaux et al, 2006;Rothwell et al, 1997;Swartz et al, 2001;Touzani et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

In vivo imaging of brain lesions with [¹¹C]CLINME, a new PET radioligand of peripheral benzodiazepine receptors

Boutin

Chauveau

Thominiaux

et al. 2007

Glia

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The peripheral benzodiazepine receptor (PBR) is expressed by microglial cells in many neuropathologies involving neuroinflammation. PK11195, the reference compound for PBR, is used for positron emission tomography (PET) imaging but has a limited capacity to quantify PBR expression. Here we describe the new PBR ligand CLINME as an alternative to PK11195. In vitro and in vivo imaging properties of [(11)C]CLINME were studied in a rat model of local acute neuroinflammation, and compared with the reference compound [(11)C]PK11195, using autoradiography and PET imaging. Immunohistochemistry study was performed to validate the imaging data. [(11)C]CLINME exhibited a higher contrast between the PBR-expressing lesion site and the intact side of the same rat brain than [(11)C]PK11195 (2.14 +/- 0.09 vs. 1.62 +/- 0.05 fold increase, respectively). The difference was due to a lower uptake for [(11)C]CLINME than for [(11)C]PK11195 in the non-inflammatory part of the brain in which PBR was not expressed, while uptake levels in the lesion were similar for both tracers. Tracer localization correlated well with that of activated microglial cells, demonstrated by immunohistochemistry and PBR expression detected by autoradiography. Modeling using the simplified tissue reference model showed that R(1) was similar for both ligands (R(1) approximately 1), with [(11)C]CLINME exhibiting a higher binding potential than [(11)C]PK11195 (1.07 +/- 0.30 vs. 0.66 +/- 0.15). The results show that [(11)C]CLINME performs better than [(11)C]PK11195 in this model. Further studies of this new compound should be carried out to better define its capacity to overcome the limitations of [(11)C]PK11195 for PBR PET imaging.

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Differential Release of Interleukines 6, 8, and 10 in Cerebrospinal Fluid and Plasma After Traumatic Brain Injury

Cited by 121 publications

References 0 publications

Serum IL-6, IL-8 and IL-10 Levels in Multiple Trauma Compared to Traumatic Brain Injury and Combined Trauma

Serum IL-6, IL-8 and IL-10 Levels in Multiple Trauma Compared to Traumatic Brain Injury and Combined Trauma

Evaluation of tgf β1, il-8 and nitric oxide in the serum of diffuse axonal injury patients and its association with clinical status and outcome

In vivo imaging of brain lesions with [¹¹C]CLINME, a new PET radioligand of peripheral benzodiazepine receptors

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Differential Release of Interleukines 6, 8, and 10 in Cerebrospinal Fluid and Plasma After Traumatic Brain Injury

Cited by 121 publications

References 0 publications

Serum IL-6, IL-8 and IL-10 Levels in Multiple Trauma Compared to Traumatic Brain Injury and Combined Trauma

Serum IL-6, IL-8 and IL-10 Levels in Multiple Trauma Compared to Traumatic Brain Injury and Combined Trauma

Evaluation of tgf &#946;1, il-8 and nitric oxide in the serum of diffuse axonal injury patients and its association with clinical status and outcome

In vivo imaging of brain lesions with [11C]CLINME, a new PET radioligand of peripheral benzodiazepine receptors

Contact Info

Product

Resources

About

Evaluation of tgf β1, il-8 and nitric oxide in the serum of diffuse axonal injury patients and its association with clinical status and outcome

In vivo imaging of brain lesions with [¹¹C]CLINME, a new PET radioligand of peripheral benzodiazepine receptors