Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case report of encephalopathy associated with Salmonella urbana infection in a child. A 5-year-old boy was admitted to our clinic with convulsions and coma. Cerebrospinal fluid (CSF) interleukin-6 (IL-6) and IL-8 were elevated at onset and were decreased within normal limit on the fifth day. Residual neurological deficits included severe mental deficits and spastic tetraplegia. High levels of CSF proinflammatory cytokines might be related to central nervous system (CNS) disease activity. Although encephalopathy is a rare complication of non-typhi Salmonella infection, it should be borne in mind as an occasionally serious and potentially lethal disease.
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PMID:Cerebrospinal fluid cytokines in Salmonella urbana encephalopathy. 1521 48

Bacterial meningitis is still associated with high mortality rate and severe neurological sequels. The aim of the study was to assess correlation between concentration of proinflammatory cytokines (TNF-alpha, IL-1 beta, IL-8) in the cerebrospinal fluid (CSF) and patient condition described on the basis of Glasgow Coma Scale (GCS), changes in the CSF (pleocytosis, protein and glucose level), mortality rate and occurrence of neurological complications. 42 patients with bacterial meningitis have been analysed. Control group consisted of 25 patients with viral meningitis and 23 patients without meningitis. In analysed group with bacterial meningitis the correlation between number of scores aggregated by patients in GCS and outcome has been observed. Concentration of TNF-alpha, IL-1 beta, IL-8 in CSF of patient with bacterial meningitis was significantly higher (mean value; 705.2 pg/ml, 401.1 pg/ml and 1696.0 pg/ml) than in control group (viral meningitis: 7.93 pg/ml, 31.89 pg/ml, 405.28 pg/ml, without meningitis: 0.38 pg/ml, 2.55 pg/ml, 32.56 pg/ml). Negative correlation between concentration of investigated cytokines in the CSF of patient with bacterial meningitis and GCS has been observed. Furthermore TNF-alpha and IL-8 levels correlated with pleocytosis, and protein and glucose levels, whereas IL-1 beta correlated with pleocytosis and protein level in CSF. Connection between TNF-alpha and IL-1 beta but not IL-8 level and outcome of bacterial meningitis has been observed. High TNF-alpha in the CSF (median value 953 pg/ml) was associated with significant risk of patient death. IL-1 beta has been better prognostic indicator. Patients who developed neurological sequels had median value of IL-1 beta level 401.3 pg/ml, and those who died had 585.9 pg/ml vs 244.7 pg/ml in the group who survived without any complications. Analysis of the ROC curve-revealed, that concentration of IL-1 beta > or = 289.9 pg/ml with 88.9% sensitivity and 67.7% specifity differentiate cases who at risk for death. For TNF-alpha the cut-off was > or = 538.9 pg/ml. The sensitivity for determined critical point was 77%, and specificity was 68.7%. Our investigation confirm that TNF alpha, IL-1 beta, IL-8 are useful in differential diagnosis of neuroinfections. Assessment of patients with bacterial meningitis on the basis of GCS is helpful to establish prognosis, and CGS seems to correlate with the intensity of inflammation in the CSF. High concentration of TNF-alpha, and IL-1 beta in the CSF are associated with the risk of patient death during the course of bacterial meningitis, but IL-1 beta has been the better prognostic marker.
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PMID:[Concentration of proinflammatory cytokines (TNF-alpha, IL-8) in the cerebrospinal fluid and the course of bacterial meningitis]. 1523 Jan 46

S100B protein (S100B) has been described as a marker of brain injury. Various cytokines also increase in the cerebrospinal fluid (CSF) of patients with severe traumatic brain injury (TBI). Thus, we investigated early changes in the concentrations of CSF S100B and various cytokines after TBI and evaluated the relations of both S100B and cytokines to intracranial pressure (ICP) and prognosis. Twenty-three patients with severe TBI and a Glasgow Coma Scale score of 8 or less on admission were included in this study. CSF and serum samples were obtained on admission and at 6, 12, 24, 48, 72, and 96 h after injury. CSF concentrations of S100B and CSF and serum concentrations of five cytokines (IL-1beta, TNF-alpha, IL-6, IL-8, and IL-10) were measured and compared. The CSF S100B concentration was increased for 6 h after injury and decreased thereafter. The CSF concentrations of IL-6 and IL-8 peaked within 6 h after injury; other cytokines (IL-1beta, TNF-alpha, and IL-10) were elevated for 24 h after injury and gradually decreased thereafter. Peak CSF S100B concentrations correlated significantly with ICP determined at the time CSF samples were taken (r = 0.729, P < 0.0001). For the cytokines investigated, only the peak CSF IL-1beta concentration correlated significantly and positively with the peak CSF S100B concentration (r = 0.397, P < 0.005). Peak CSF concentrations of S100B (1649 +/- 415 microg/L, mean +/- SEM) and IL-1beta (16.5 +/- 3.3 pg/mL) in the 6 patients with high ICP were significantly higher than those (233 +/- 67 microg/L, 7.6 +/- 1.7 pg/mL, respectively) in the 17 patients with low ICP (P < 0.05). The CSF S100B concentration (1231 +/- 378 microg/L) in eight patients with an unfavorable outcome was significantly higher than that (267 +/- 108 microg/L) in 15 patients with a favorable outcome (P < 0.05). The CSF IL-1beta concentration (14.8 +/- 3.4 pg/mL) in eight patients with an unfavorable outcome tended to be higher than that (7.3 +/- 1.5 pg/mL) in 15 patients with a favorable outcome (P = 0.057). CSF concentrations of S100B and cytokines peak within 24 h after severe TBI and decrease gradually thereafter. CSF S100B and IL-1beta may be useful as predictors of outcome in cases of severe TBI.
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PMID:Changes in CSF S100B and cytokine concentrations in early-phase severe traumatic brain injury. 1525 81

The aim of this study was to evaluate the relation between severity of injury and the early activation of interleukins in multiple-injured patients. Ninety-nine patients with multiple injuries were included in this prospective study. Plasma levels of interleukin (IL)-1, IL-2, IL-6, IL-8 and TNF-alpha were measured. Injury Severity Score (ISS), Revised Trauma Score (RTS), Glasgow Coma Score (GCS) and the Acute Physiology and Chronic Health Evaluation II (APACHE-II) were all recorded. Of the 99 patients, 82 were male and 17 were female. The mean age was 26.6+/-20.7 years. The mortality rate for this series was 17%. Patients who died from trauma exhibited a significant increase for IL-2, IL-6 and IL-8 in comparison with patients who survived. Significant differences for ISS, RTS and GCS were found between survivors and non-survivors. Values in all patients with ISS>16 were increased and these increases were significant for IL-6 and IL-2. These data show that the initial increase of IL-2, IL-6 and IL-8 might predict the patients with a high possibility of mortality and a significant increase of IL-2 and IL-6 in patients with ISS>16 might be used in a new developed trauma score combined with ISS as an indicator for the injury severity.
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PMID:Relation between severity of injury and the early activation of interleukins in multiple-injured patients. 1646 61

Traumatic brain injury (TBI) acts as an inducer of the inflammatory reaction expressed by the release of pro-inflammatory cytokines (interleukin-1beta [IL-1beta], interleukin-6 [IL-6] and interleukin-8 [IL-8]), and causes metabolic alterations in the early, post-traumatic state, either in the brain or/and the systemic circulation. The metabolic changes involve carbohydrates, proteins and lipids. We focused on the serum lipid profile, the impact of trauma on lipoproteins, and their subsequent effects, on inflammation. We investigated the role of cytokines and serum lipids, in patient outcome, reviewing 30-day mortality and the Glasgow Coma Scale (GCS). A total of 75 patients with severe or moderate TBI (GCS <or= 13) were allocated to two groups (group 1 non-survivors and group 2 survivors). One blood sample was collected from each patient within 24h of admission. Cytokines were measured in serum by ELISA and serum lipids using an enzymatic method. We found significantly decreased serum lipid levels and increased cytokines levels for all patients compared with healthy volunteers. Comparing the two groups, IL-6 and IL-8 levels were higher (p<0.0001) and LDL levels lower (p=0.003) in non-survivors than in survivors. We observed a significant inverse correlation between IL-8 and LDL (p=0.04) in patients with an unfavorable outcome. Our results suggest that LDL alone, or in combination with IL-6 and IL-8, could be a possible prognostic factor for outcome in patients with TBI, as regards 30- day mortality.
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PMID:Hypolipoproteinemia and hyperinflammatory cytokines in serum of severe and moderate traumatic brain injury (TBI) patients. 1799 53

This study performed a comprehensive analysis of cerebrospinal fluid (CSF) cytokine levels after severe traumatic brain injury (TBI) in children using a multiplex bead array assay and to evaluate the effects of moderate hypothermia on cytokine levels. To this end, samples were collected during two prospective randomized controlled trials of therapeutic moderate hypothermia in pediatric TBI. Thirty-six children with severe TBI (Glasgow Coma Scale [GCS] score of <or=8) and 10 children with negative diagnostic lumbar punctures. All children with TBI had continuous monitoring of intracranial pressure and CSF drainage via an intraventricular catheter. Moderate hypothermia (32-33 degrees C) was maintained for 48 h in 17 patients, and they were slowly re-warmed at 48-72 h. A multiplex bead array assay was used to analyze serial CSF samples (<18 h, 24 +/- 6 h, 48 +/- 6 h, and 72 +/- 6 h) for 21 pro-and anti-inflammatory cytokines and chemokines. Interleukin (IL)-8 and transforming growth factor beta were measured by enzyme-linked immunosorbant assay (ELISA). There was a strong correlation (Spearman correlation coefficient = 0.92, p < 0.001) between multiplex assay and ELISA for IL-8. Pro-inflammatory IL-1beta, -6 and -12p70, anti-inflammatory IL-10 and chemokines IL-8 and MIP-1alpha were increased after TBI compared to controls, p < 0.05; however, there was no association between cytokines and age, gender, initial GCS, or outcome. Hypothermia did not attenuate the increases in CSF cytokine levels after TBI versus normothermia. This investigation confirmed that the multiplex bead array assay is a useful method to measure CSF cytokine levels. Severe TBI in infants and children induces increases in pro- and anti-inflammatory cytokines and chemokines. It is the first clinical report of increased levels of MIP-1alpha after TBI in any patient population and the most comprehensive assessment of cytokines after TBI to date. Moderate therapeutic hypothermia did not attenuate the increase in CSF cytokine levels in children after TBI.
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PMID:Multiplex assessment of cytokine and chemokine levels in cerebrospinal fluid following severe pediatric traumatic brain injury: effects of moderate hypothermia. 1800 Dec 1

Although multiple organ failure (MOF) remains the leading cause of death after trauma, the pathogenic cellular and molecular mechanisms underlying MOF are poorly understood. In addition to proinflammatory and anti-inflammatory mediator cascades, the temporal onset of MOF has generated recent interest because the organ systems involved into MOF seem to deteriorate in a time-dependent fashion after trauma. We therefore investigated the temporal course of MOF in traumatized human patients and evaluated and compared the distribution patterns of cytokine expression, including interleukin (IL) 6, IL-8, IL-10, and the soluble tumor necrosis factor-[alpha] receptors sTNF-R p55 and sTNF-R p75 in early-onset versus late-onset MOF. In addition, we analyzed the predictive value of cytokine biomarkers of MOF and lethal outcome. In a prospective observational cohort study conducted at three trauma centers, all patients (n = 352) admitted to two level 1 trauma centers in Germany were enrolled in the study based on the following inclusion criteria: severe traumatic brain injury (TBI) with a Glasgow Coma Scale (GCS) score of 8 or lower and/or distinct changes in cranial computed tomography and/or multiple injuries (MT) to the body (at least two regions had Abbreviated Injury Scale score of 3 or higher). The incidence of MOF was evaluated using the modified Goris-MOF score. The temporal onset of MOF was divided into early-onset MOF (EMOF, developing on days 0-3), late-onset MOF (LMOF, developing on days 4-10), combined early-onset and late-onset MOF (CMOF), and patients never showing signs of MOF during the observation period. In addition, the levels of the serum cytokine markers IL-6, IL-8, IL-10, sTNF-R p55, and sTNF-R p75 were analyzed at specific posttraumatic time points using established enzyme-linked immunosorbent assay techniques. A total of 352 patients (274 men and 78 women; TBI, 101; TBI + MT, 125; MT, 126) were enrolled into the study. Patients assigned to the EMOF group showed specific disruption of pulmonary and cardiocirculatory function, whereas LMOF was significantly associated with hepatic failure. The patients without signs of MOF and the EMOF patients had the same risk of lethal outcome (8.2% vs. 7.5%); LMOF and CMOF were found to be associated with a 3- to 4-fold increase in mortality (38.5% vs. 30.6%, respectively). Analysis of cytokine serum biomarkers revealed that patients with LMOF showed a biphasic elevation of IL-6 and significantly higher sTNF-R concentrations than did all other subgroups (P < 0.001). In addition, the initial values (days 0-1) of sTNF-R p55 and sTNF-R p75 expression levels had a good predictive capacity for the development of LMOF (p55, 0.75; p75, 0.72); values greater than 0.65 were accepted to have a predictive capacity. These results demonstrate that mortality differs significantly between the development of EMOF and LMOF after traumatic injury. Our results also suggest that serum cytokine measurements may be important early biochemical markers for predicting the development of delayed MOF.
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PMID:Early versus late onset of multiple organ failure is associated with differing patterns of plasma cytokine biomarker expression and outcome after severe trauma. 1809 84

Cerebral malaria is a severe multifactorial condition associated with the interaction of high numbers of infected erythrocytes to human brain endothelium without invasion into the brain. The result is coma and seizures with death in more than 20% of cases. Because the brain endothelium is at the interface of these processes, we investigated the global gene responses of human brain endothelium after the interaction with Plasmodium falciparum-infected erythrocytes with either high- or low-binding phenotypes. The most significantly up-regulated transcripts were found in gene ontology groups comprising the immune response, apoptosis and antiapoptosis, inflammatory response, cell-cell signaling, and signal transduction and nuclear factor kappaB (NF-kappaB) activation cascade. The proinflammatory NF-kappaB pathway was central to the regulation of the P falciparum-modulated endothelium transcriptome. The proinflammatory molecules, for example, CCL20, CXCL1, CXCL2, IL-6, and IL-8, were increased more than 100-fold, suggesting an important role of blood-brain barrier (BBB) endothelium in the innate defense during P falciparum-infected erythrocyte (Pf-IRBC) sequestration. However, some of these diffusible molecules could have reversible effects on brain tissue and thus on neurologic function. The inflammatory pathways were validated by direct measurement of proteins in brain endothelial supernatants. This study delineates the strong inflammatory component of human brain endothelium contributing to cerebral malaria.
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PMID:Plasmodium falciparum-infected erythrocytes induce NF-kappaB regulated inflammatory pathways in human cerebral endothelium. 1971 60

This study aims to determine if pairing the Glasgow Coma Scale (GCS) with serum biomarker levels may achieve higher outcome predictive values than using either the GCS or biomarker levels alone in childhood brain trauma. Twenty-eight critically ill children with isolated accidental brain trauma were studied in a prospective observational study. The GCS was recorded at various time points post injury. Enzyme-linked immunosorbent assay (ELISA) was used to quantify eight different serum biomarker levels (S100b, NSE, IL-6, IL-8, IL-10, L-selectin, SICAM, and endothelin) on day 1 post injury. The Glasgow Outcome Score (GOS) was used to assess global outcome at 6 months post injury. Outcome predictive values of the GCS, individual biomarker levels, and paired combinations of the GCS and biomarkers were compared using receiver operator characteristic (ROC) curve analysis and its multivariate extension, multivariate ROC curve (MultiROC). When using either the GCS or individual biomarker levels alone to predict unfavorable outcome, only the PICU discharge summated GCS achieved an area under the ROC curve (AUC) of more than 0.95. This high degree of outcome predictability was also achieved by pairing the GCS with a single biomarker level. The most pronounced improvement in outcome prediction was observed by pairing the post-resuscitation summated GCS with the day-1 serum IL-8 level, which increased the AUC from 0.78 to 0.98 and the sensitivity and specificity from 75% to 100% and 96% respectively. Paired combinations of the GCS and serum biomarker levels greatly enhanced the accuracy of post-traumatic unfavorable outcome prediction than may be achieved using either the GCS or individual biomarker levels alone.
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PMID:Combining coma score and serum biomarker levels to predict unfavorable outcome following childhood brain trauma. 2085 21

This study evaluated serum neuron-specific enolase (NSE), cytokine and high-sensitivity C-reactive-protein (hs-CRP) levels, along with the Glasgow Coma Scale (GCS) and Revised Trauma Score (RTS), as predictors of mortality in the early posttraumatic period, in 100 Turkish patients with blunt head trauma. Overall patient mortality was 27%. There was a significant association between age and mortality, and mortality was negatively correlated with GCS and RTS. Head injury severity (GCS) was significantly related to NSE, hs-CRP, interleukin (IL)-6, IL-8 and tumour necrosis factor (TNF)-alpha levels. Mortality correlated positively with IL-6, IL-8, TNF-alpha and hs-CRP levels. NSE, hs-CRP, IL-6, IL-8 and TNF-alpha levels were significantly higher in non-survivors compared with survivors. GCS score < or =8, younger age and NSE levels were significant independent predictors of mortality. During the early post-traumatic period, NSE may be an objective alternative criterion to the GCS, in the management of patients with blunt head trauma.
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PMID:Trauma scores and neuron-specific enolase, cytokine and C-reactive protein levels as predictors of mortality in patients with blunt head trauma. 2130 85


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