interleukin-8 and Craniocerebral-Trauma

Patients with head injury must overcome central as well as peripheral metabolic insults. In addition to specific tissue damage to the brain, a cellular biochemical cascade occurs that can negatively affect organ function, cause a systemic response to injury, and may cause secondary tissue injury. The metabolites involved in this cascade are numerous and complex. Cytokines are important cell-to-cell communication mediators during injury. It is speculated that cytokines, such as interleukin 1 (IL-1), interleukin 6 (IL-6), tumor necrosis factor (TNF), and interleukin 8 (IL-8), which are found in elevated amounts in both human and basic trials after head injury, play a role in the cellular cascade of injury. Some of the metabolic events produced by small doses of cytokine infusion in animals, as well as humans, include fever, neutrophilia, muscle breakdown, altered amino acid metabolism, depression of serum zinc levels, production of hepatic acute phase reactants, increased endothelial permeability, and expression of endothelial adhesion molecules. These are all known sequelae of severe head injury. Cytokines have also been implicated in organ failure. Infusion of cytokines in basic science trials revealed that organ functions of the gut, liver, and lung are negatively altered by high-dose cytokine infusion. Infusion of certain cytokines has been shown to cause death of brain cells, increase blood-brain barrier permeability, and cause cerebral edema. This suggests that cytokines may also play a role in the sequelae of organ demise. These effects of cytokines have been attenuated in basic trials by blocking the initial signaling system of cytokines or by decreasing serum cytokine activity. We hypothesize that cytokines that are elevated after head injury play a role in the pathology of injury, including altered metabolism and organ demise.

Topics: Animals; Craniocerebral Trauma; Cytokines; Gastrointestinal Diseases; Humans; Interleukin-1; Interleukin-6; Interleukin-8; Liver Diseases; Lung Diseases; Rabbits; Tumor Necrosis Factor-alpha

To explore whether transplantation of bone marrow mesenchymal stem cells (BMSCs) would reduce the immune response and protect vital organs in a rat model of femur shaft fracture combined with craniocerebral injury.. The rats were divided into an experimental group (multiple traumas and receiving BMSCs injection, n = 25), a positive control group (only received the combination injuries, n = 25) and a negative group (n = 5).. Compared with the positive control group, plasma IL-6 and IL-8 were significantly lower at the early stage, and IL-10 was higher at the late period in the experimental group (p < 0.05). TNF-α ex-vivo synthesis descended quickly after trauma.. BMSCs reduced the inflammatory response and were effective in immunomodulations during severe trauma.

Topics: Animals; Bone Marrow; Cells, Cultured; Craniocerebral Trauma; Disease Models, Animal; Femoral Fractures; Humans; Immunomodulation; Inflammation Mediators; Interleukin-10; Interleukin-6; Interleukin-8; Male; Mesenchymal Stem Cells; Multiple Trauma; Rats; Rats, Sprague-Dawley

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.. 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).. 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).. 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.

Topics: Adult; Craniocerebral Trauma; Cross-Sectional Studies; Diffuse Axonal Injury; Glasgow Coma Scale; Glasgow Outcome Scale; Humans; Interleukin-8; Male; Multiple Trauma; Nitric Oxide; Transforming Growth Factor beta1; Treatment Outcome

Estimation of trauma severity currently relies on clinical diagnoses and scoring systems. However, the early estimation of the severity of chest trauma and overall soft tissue trauma (STT) remains insufficient. Traditional trauma scoring systems fail to reflect the individual trauma pattern and severity, neglecting the different outcomes after injuries in different body regions. Therefore, the aim of this prospective study was to detect laboratory markers that may reflect the pattern and extent of individual trauma in the very early phase after injury.. In 107 non-selected trauma patients, blood samples were collected almost immediately and then at short intervals after the trauma. In addition to the biochemical analysis of 20 different mediators viewed as potential trauma markers, the following data were correlated with the laboratory results: injury severity score (ISS), polytrauma score (PTS), Ulmer score HTAPE (trauma pattern specific: head (H), thorax (T), abdomen (A), pelvis (P), extremities (E); 0-3 degrees each), multiple organ failure score (MOF), overall, primary and secondary lethality.. ISS and the severity of head injury were clearly higher in non-survivors (n=17) than in survivors (n=90) (median ISS: 35 versus 18; median severity of head injury (H): 3 versus 1). Whereas head injury was correlated with early death (3 days post-trauma) was influenced by thoracic trauma (r=0.15) as well as by soft tissue trauma (STT, r=0.12). Of all investigated mediators, interleukin-6 (IL-6) displayed the highest correlations (r=0.66, P<0.00001) with the extent of chest trauma, followed by correlations with PTS, STT, fracture trauma (FT) and ISS during the first hour after trauma. There was no correlation between IL-6 and head injury. The extent of STT was correlated best to IL-8 (r=0.75), IL-6 (r=0.54), and creatine kinase (CK, r=0.49) plasma concentrations.. In the very early stage after an accident the severity of chest trauma is strongly correlated with the plasma concentration of IL-6, and the extent of overall soft tissue trauma (STT) to plasma concentrations of IL-8, IL-6, and CK.

Topics: Adolescent; Adult; Aged; Biomarkers; Craniocerebral Trauma; Creatine Kinase; Female; Humans; Interleukin-6; Interleukin-8; Male; Middle Aged; Multiple Organ Failure; Prospective Studies; Soft Tissue Injuries; Statistics, Nonparametric; Survival Rate; Thoracic Injuries; Trauma Severity Indices; Wounds and Injuries

Severe neurological deficits are common characteristics of patients surviving cardiopulmonary resuscitation (CPR) or isolated severe head trauma (SHT). For comparative evaluation of underlying pathomechanisms, 22 patients with out-of-hospital cardiac arrest and successful CPR as well as 10 patients with SHT were included in our prospective study. Circulating S-100B was determined as an indicator of cellular brain damage. Interleukin-8 (IL-8), soluble E-selectin (sE-selectin) and polymorphonuclear (PMN-) elastase were measured as markers of systemic inflammation following whole body ischaemia and reperfusion injury. Venous blood samples were drawn on scene (median time 11.0 min after starting basic life support) and in the intensive care unit (median time 12.5 h thereafter) in CPR patients and at admission to hospital (median time 43.8 min after trauma) and approx. 12 h later in SHT patients. Biochemical parameters in these samples were compared with specimens taken from 20 healthy volunteers. Initial median S-100B levels of the CPR and SHT patients were both significantly increased compared with the controls. Twelve hours later, significant falls in S-100B revealed no differences between the two patient groups, but did not reach control values. Median IL-8 and sE-selectin levels entry to the study were elevated in both patient groups compared with controls and showed further rises within the following 12 h. Finally, increased initial median levels of PMN-elastase revealed significant differences between the patient groups and between patients and controls. Twelve hours later, median PMN-elastase values were equally elevated in the CPR and SHT subjects. Our preliminary data suggest similar pathomechanisms occurring after both CPR and SHT. Both clinical entities seem to be associated with early transient cellular brain damage as shown by prolonged rapidly increasing and subsequent fall in S-100B serum levels. In contrast, the prolonged elevation of circulating IL-8, sE-selectin and PMN-elastase may indicate a very similar systemic inflammatory response by endothelial cells and neutrophils initiated by ischaemia and reperfusion injury in both conditions. Further studies should be carried out to determine the cause and the prognostic value of these biochemical parameters in relation to long-term neurological outcome.

Topics: Aged; Brain; Brain Damage, Chronic; Calcium-Binding Proteins; Cardiopulmonary Resuscitation; Craniocerebral Trauma; E-Selectin; Female; Humans; Inflammation; Interleukin-8; Leukocyte Elastase; Male; Middle Aged; Nerve Growth Factors; Pilot Projects; Prospective Studies; Reference Values; S100 Calcium Binding Protein beta Subunit; S100 Proteins; Time Factors

To determine interleukin (IL)-8 concentrations in ventricular cerebrospinal fluid from children with severe traumatic brain injury (TBI).. Prospective study.. University children's hospital.. Twenty-seven children hospitalized with severe TBI (Glasgow Coma Scale score < or =8), seven children with cerebrospinal fluid culture-positive bacterial meningitis, and twenty-four age-equivalent controls.. Placement of an intraventricular catheter and continuous drainage of cerebrospinal fluid.. Median [range] cerebrospinal fluid IL-8 concentration in children with TBI (0-12 hrs) (4,452.5 [0-20,000] pg/mL) was markedly greater than that in controls (14.5 [0-250]) (p < .0001) and equivalent to concentrations in children with meningitis (5,300 [1,510-22,000] pg/mL) (p = .33). Cerebrospinal fluid IL-8 remained increased in children with severe TBI for up to 108 hrs after injury. Univariate logistic regression analysis demonstrated an association between cerebrospinal fluid IL-8 and child abuse (p = .07) and mortality (p = .01). Multivariate analysis demonstrated a strong, independent association between cerebrospinal fluid IL-8 and mortality (p = .01).. The data are consistent with an acute inflammatory component of TBI in children and suggest an association between cerebrospinal fluid IL-8 and outcome after TBI. IL-8 may represent a potential target for anti-inflammatory therapy.

Topics: Acute Disease; Adolescent; Biomarkers; Child; Child, Preschool; Craniocerebral Trauma; Enzyme-Linked Immunosorbent Assay; Female; Humans; Infant; Interleukin-8; Logistic Models; Male; Meningitis, Bacterial; Prospective Studies; Time Factors

The adult respiratory distress syndrome (ARDS) is a frequent complication after severe accidental trauma. This study examines the hypothesis that increased systemic concentrations of proinflammatory cytokines, endotoxin, or complement fragments may predict the development of ARDS.. Prospective, observational study.. Two Level I university trauma centers.. Fifteen severely injured patients (Injury Severity Score of > or = 25).. Standard emergency department, operating room, and intensive care unit management.. Plasma samples were obtained at 4-hr intervals from the time of injury and were assayed for concentrations of endotoxin, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-8, and complement fragments C3a and C4a. Hemodynamic and oxygen metabolism variables also were measured at 4-hr intervals after injury. Seven patients developed ARDS and eight patients did not. The PaO2/FIO2 ratio was significantly decreased in the patients with ARDS compared with non-ARDS patients as early as 4 hrs postinjury, and remained significantly decreased throughout the initial 24 hrs after severe accidental injury. Plasma IL-8, IL-6, C3a, and C4a concentrations were markedly increased starting in the immediate postinjury period in both ARDS and non-ARDS patients, but no significant differences were found between the two groups until 16 hrs after injury when plasma IL-8, C3a, and C4a concentrations became significantly higher in the ARDS group. Neither the ARDS nor non-ARDS patients showed the presence of circulating IL-1 beta, TNF-alpha, or endotoxin at any postinjury time point.. These results demonstrate that measurements of plasma concentrations of proinflammatory cytokines, endotoxin, or complement fragments are not helpful in predicting the development of ARDS after severe accidental injury.

Topics: Adult; Blood Gas Analysis; Complement C3a; Complement C4a; Craniocerebral Trauma; Endotoxins; Enzyme-Linked Immunosorbent Assay; Female; Hemodynamics; Humans; Injury Severity Score; Interleukin-1; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Oxygen Consumption; Peptide Fragments; Predictive Value of Tests; Prognosis; Prospective Studies; Radioimmunoassay; Respiratory Distress Syndrome; Risk Factors; Survival Rate; Time Factors; Tumor Necrosis Factor-alpha