Plasma Levels Of Interleukin-1 Beta Research Articles

Novel Biomarkers in Evaluating Cardiac Function in Patients on Hemodialysis-A Pilot Prospective Observational Cohort Study.

Chronic kidney disease patients treated by hemodialysis present a high cardiovascular morbidity and mortality. There is an imperative need for novel biomarkers for identifying these patients and to offer possible therapeutically interventions. We performed a prospective observational cohort study on 77 patients in the period of October 2021-October 2023. We measured serum plasma levels of interleukin 1-beta, galectin 3, human suppression of tumorigenicity factor 2, bone morphogenetic protein 2 and fibroblastic growth factor 23 at the inclusion site. We evaluated the correlations of these biomarkers with cardiac function and structure evaluated by echocardiography. The mean age was 61.02 (±11.81) years, with 45 (56.2%) males and with a dialysis vintage of 4.95 (2.4-7.8) years. Median ejection fraction was 51 (43-54%), and more than two-thirds of the patients presented valvular calcifications. Overall mortality was 22%. Interleukin 1-beta was correlated positively with ejection fraction and global longitudinal strain and negatively with left atrium diameter and left ventricle telesystolic diameter. Galectin 3 values were negatively correlated with aortic valve fibrosis and mitral valve calcifications, and human suppression tumorigenicity factor 2 was negatively correlated with mitral valve calcifications. Some of these novel biomarkers could be used to better assess cardiovascular disease in patients on maintenance hemodialysis.

Increased plasma levels of IL-6 are associated with striatal structural atrophy in major depressive disorder patients with anhedonia.

Anhedonia, as the core endophenotype of major depressive disorder (MDD), is closely related to poor prognosis, but the mechanism of this feature remains to be understood. The aim of this study was to investigate the inflammatory factors and brain structural alterations in MDD patients with anhedonia and evaluate the relationship between these factors. We assessed the plasma levels of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in MDD patients with anhedonia (n = 22), MDD patients without anhedonia (n = 20), and age- and sex-matched healthy controls (HCs, n = 20) by enzyme-linked immunosorbent assay kits. All participants underwent high-resolution brain magnetic resonance imaging (MRI) scans, and voxel-based morphometry (VBM) was used to evaluate their gray matter volume (GMV). We compared inflammatory factors and GMV among the three groups and explored their relationships in MDD patients with anhedonia. Compared with those of HCs, plasma levels of IL-1β were increased in patients with MDD independent of anhedonia features, while plasma levels of IL-6 were elevated in MDD patients with anhedonia only. Meanwhile, MDD patients with anhedonia exhibited reduced GMV in the left striatal structures compared to MDD patients without anhedonia and HCs. Moreover, a significant association was observed between increased plasma levels of IL-6 and decreased GMV of the left putamen in MDD patients with anhedonia. The present research outcomes suggest that anhedonia is associated with increased plasma levels of IL-6 and decreased GMV in the left striatal structures. In addition, this study demonstrates that GMV loss in the left putamen is related to increased plasma levels of IL-6 in MDD with anhedonia, which provides further insights into the possible mechanisms of anhedonia.

P 11 Hydrogen peroxide-induced inflammation and decreased vitamin D receptor in placental explants

Introduction Placental oxidative stress has been associated with the pathogenesis of preeclampsia (PE). The imbalance between pro- and anti-inflammatory cytokines in this pathology could be explained by the deficiency of regulatory factors capable of modulating this inflammatory state. Vitamin D may act as anti-inflammatory agent, by regulating the production of inflammatory cytokines and generating an immune tolerogenic environment. Objectives The present study evaluated whether there is association between plasma levels of vitamin D and cytokines, as well as gene expression of vitamin D receptor (VDR) and pro-and anti-inflammatory cytokines by placental explants obtained from normotensive (NT) pregnant women, from women with PE and from NT pregnant women explants treated with or without hydrogen peroxide (H2O2). Methods Blood of 20 PE and 20 NT were collected and plasma concentrations of 25-hydroxyvitamin D [25(OH) D] was evaluated by chemiluminescence. Plasma levels of Interleukin-1 beta (IL-1β), IL-10 and tumor necrosis fator alpha (TNF-α) were detected by ELISA. Placental explants from 15 NT pregnant and 15 PE women in the third trimester of pregnancy were obtained from women undergoing elective cesarean section. NT placental explants were cultured with or without 100 μM H2O2 for 4 h. The gene expression of cytokines (IL-1β, IL-10 and TNF-α) and VDR were determined by qPCR. Differences between groups were analyzed by non-parametric tests with significant level set at 5%. Results Plasma concentration of 25(OH) D and IL-10 was significantly lower in PE group than in the NT group, while levels of TNF-α and IL-1β were higher in PE group. Gene expression of VDR was lower in explants from PE group and in the NT group with H2O2. Gene expression of TNF-α and IL-1β were significantly higher in PE and NT with H2O2. However, IL-10 levels were significantly lower in these groups when compared to normotensive group. Positive correlation between IL-10 and VDR gene expression was observed between normotensive groups (r = 0.8857; p = 0.0333). Conclusion The results showed an imbalance between vitamin D and its receptor with cytokine profile in explants from preeclamptic women as well as in placental explants obtained from NT pregnant women and submitted to oxidative stress and inflammation induced by hydrogen peroxide. Financial support – FAPESP 2016/18155–9

Evaluation of psoriasis severity and inflammatory responses under concomitant treatment with methotrexate plus micronutrients for psoriasis vulgaris: a randomized double blind trial

We evaluated the effectiveness of concomitant treatment with methotrexate (MTX) plus micronutrients in comparison with monotherapy with MTX only in psoriasis patients. Plasma levels of interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) were also measured and their association with clinical severity was evaluated. Thirty psoriasis patients 20 to 50 years old with a PASI score > 10 were divided randomly into two groups. Both groups were given oral methotrexate (0.2-0.3 mg/kg/week) for 12 weeks. In addition, Group B received one tablet of micronutrient supplement daily. Disease severity was calculated using the psoriasis area and severity index (PASI) score before and after 12 weeks. Levels of IL-1β and TNF-α were measured using enzyme-linked immunosorbent assay (ELISA). We found that 13 (86.6%) patients in Group B and 8 (53.3%) patients in Group A attained a mild PASI score (≤ 10% body involvement). IL-1β and TNF-α levels were significantly decreased in favor of Group B (p < 0.05). There was a significant correlation between changes in both IL-1β and TNF-α levels and PASI score after the study (p < 0.05). The results obtained were positive, and therefore double-blind randomized trials with a larger sample size are highly suggested to confirm or reject these results.

Plasma proinflammatory and anti-inflammatory cytokine and catecholamine concentrations as predictors of neurological outcome in acute stroke patients

Proinflammatory and anti-inflammatory cytokines may play a pivotal role in cerebral inflammation, which is implicated in the development of brain injury. Systemic cytokine release is mediated by the sympathetic nervous system and catecholamines. The aim of this study was to investigate which parameters, among plasma levels of interleukin-1beta (IL-1beta), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor alpha (TNF-alpha) and the levels of the catecholamines, epinephrine and norepinephrine, contribute to the clinical outcome in acute stroke patients. Thirty-seven acute stroke patients (ischemic, n = 19; hemorrhagic, n = 18) were enrolled. All of them were admitted to our hospital within 8 h after stroke onset. Neurological status was evaluated by a modified National Institute of Health Stroke Scale (mNIHSS) on admission and by a modified Rankin Scale (mRS) at 1 month. An mRS score of 3 or more at 1 month was considered to indicate poor outcome. Serum samples for the cytokine and catecholamine measurements were collected on admission. Plasma levels of IL-1beta, IL-6, IL-10, and TNF-alpha were determined by an enzyme-linked immunosorbent assay (ELISA) method and epinephrine and norepinephrine concentrations were determined by high-performance liquid chromatography with electrochemical detection (HPLC-EC). In the ischemic stroke patients, poor outcome was noted in 9 (47%). There were no significant differences in cytokine or catecholamine concentrations between patients with poor and good outcomes, and there was no association between clinical outcome and cytokine and catecholamine concentrations. In the hemorrhagic stroke patients, poor outcome was noted in 10 (56%). IL-6 and IL-10 levels were higher in patients with poor outcome. On logistic regression analysis, higher values of IL-6 were significantly associated with clinical outcome at 1 month (odds ratio [OR], 1.25; 95% confidence interval [CI], 1.02-1.54). In ischemic stroke, plasma cytokines and catecholamines were not predictors of neurological outcome at 1 month. In hemorrhagic stroke, high levels of IL-6 in the early phase indicated a poor neurological outcome.

Effects of N-acetylcysteine and tirilazad mesylate on intestinal functional capillary density, leukocyte adherence, mesenteric plasma extravasation and cytokine levels in experimental endotoxemia in rats

The study's objective was to determine the effects of the administration of N-acetylcysteine (NAC) and of tirilazad mesylate (TM) on intestinal functional capillary density, mesenteric plasma extravasation, leukocyte adherence and on cytokine release during experimental endotoxemia in rats. In a prospective, randomized, controlled animal study, 80 male Wistar rats were examined in 2 test series. Both series were divided into 4 groups. Group 1 served as control group (CON group). Group 2 (LPS group), group 3 (NAC group) and group 4 (TM group) received endotoxin infusions (10 mg/kg over 2 h). In NAC group 150 mg/kg body weight NAC was administered after the first 30 minutes of endotoxemia intravenously. In TM group, 10 mg/kg body weight TM was administered after the first 30 minutes of endotoxemia intravenously. Animals of the series 1 underwent studies of leukocyte adherence on submucosal venular endothelium of the small bowel wall and intestinal functional capillary density (FCD) in the intestinal mucosa and the circular as well as the longitudinal muscle layer by intravital fluorescence microscopy (IVM). Plasma levels of interleukin 1beta (IL-1beta), interferone gamma (IFN-gamma) and soluble intercellular adhesion molecule1 (s-ICAM 1) as well as white blood cell count (WBC) were estimated. In the animals of the series 2 mesenteric plasma extravasation was determined by IVM and plasma levels of tumor necrosis factor alpha (TNF-alpha), IL-4, IL-6, IL-10 and malondialdehyde (MDA) were estimated. After LPS administration, FCD in the villi intestinales was unchanged and in the longitudinal muscularis layer it was increased. There was no effect of NAC or TM administration on FCD.Although the plasma extravasation was not significantly influenced by LPS administration, TM administration resulted in a lower plasma extravasation in the TM group compared to the other groups. After endotoxin challenge, the firmly adherence of leukocytes to vascular endothelium as a parameter of leukocyte activation in endotoxemia was increased but NAC or TM administration had no influence on leukocyte adherence. The plasma levels of IL-1beta, IL-6, IL-10, TNF-alpha, IFN-gamma and sICAM-1 were increased in the endotoxemic groups (LPS group, NAC group and TM group) and the WBC was decreased compared to controls. IL-4 levels were unchanged during observation period. Plasma MDA levels were not influenced by LPS administration compared to controls. The administration of NAC resulted in lower sICAM-1 and MDA levels compared to the LPS group. The IL-1beta, IL-6, IL-10, TNF-alpha and IFN-gamma plasma levels were not influenced by NAC or TM administration. In this posttreatment sepsis model in rats, NAC administration resulted in lower sICAM-1 and MDA levels compared to the LPS treated animals. TM administration reduced the plasma extravasation in this model.

Inflammation and apoptosis genes and the risk of restenosis after percutaneous coronary intervention

Genetic factors appear to be important in the development of restenosis after percutaneous coronary intervention, as well as in the process of inflammation, a pivotal factor in restenosis. Caspase-1, interleukin-1-receptor and protein tyrosine phosphatase nonreceptor type 22 are important mediators in the inflammatory response and caspase-1 also in apoptosis. Therefore, we examined whether polymorphisms in these candidate genes are related to the risk of developing restenosis after percutaneous coronary intervention. The GENetic DEterminants of Restenosis-project is a multicenter prospective follow-up study. The 5352G/A (L235L) caspase-1-polymorphism, the 7464C/G (A124G) interleukin-1r-polymorphism and the 1858C/T (R620W) protein tyrosine phosphatase nonreceptor type 22-polymorphism were genotyped. To examine the functional effect of the caspase-1 polymorphism, mature plasma interleukin-1beta levels were measured by enzyme-linked immunosorbent assay in lipopolysaccharide-stimulated whole blood from a subpopulation of patients. A total of 3104 patients, age 62.1+/-10.7 years, were included after successful percutaneous coronary intervention. A significant association between the 5352AA genotype of the caspase-1 gene and target vessel revascularization (relative risk 2.2, 95% confidence interval 1.32-3.76) was observed after correcting for clinical variables. Angiographic analysis of a subgroup of patients (N=478) also showed an increased risk for developing restenosis for patients having the 5352GA/AA genotype (P=0.001). The results were corroborated, although they were not statistically significant, by somewhat higher mature interleukin-1beta levels in patients with the 5352AA genotype. The present study shows that patients with the 5352AA genotype in the caspase-1 gene are at increased risk of developing restenosis. If confirmed by other studies, screening patients for this genotype can lead to better risk stratification and provide indications for improving individual treatment; for instance, by providing a new target for drug-eluting stents.

Protection against acute porcine lung ischemia/reperfusion injury by systemic preconditioning via hind limb ischemia

Previous work on various organs and tissues has shown that ischemic preconditioning protects against reperfusion injury in these organs and also against secondary effects in the lung. In contrast, the purpose of this study was to investigate the effects of preconditioning in a remote organ (hind limb ischemia) on an ischemia/reperfusion (I/R) treatment of the lung itself. A porcine model of in situ left lung ischemia (90 min) and reperfusion (5 h) was used. Systemic preconditioning was induced by clamping the left common femoral artery (3 x 5 min). Lung injury was assessed in terms of pulmonary vascular resistance, pulmonary artery pressure, pulmonary venous and arterial pO(2), and tissue macrophage counts. The zymosan-stimulated release of reactive oxygen species (ROS) in whole blood was determined by a chemiluminometric procedure. Inflammatory cytokines (interleukin-1beta and interleukin-6) were measured in arterial plasma as indicators of a systemic inflammatory reaction. Preconditioning by hind limb ischemia completely prevented the I/R-induced functional impairment of the lung, the pulmonary hypertension and the reduced oxygenation capacity. The plasma levels of interleukin-1beta and the macrophage counts in preconditioned animals were reduced to control values, whereas the levels of interleukin-6 and the release of ROS were not affected by preconditioning. In conclusion, systemic preconditioning by repeated hind limb ischemia protects against acute I/R injury of the lung but not against all indices of reperfusion-associated systemic inflammation.

Plasma levels of interleukin-1beta, interleukin-2 and interleukin-4 in recently diagnosed type 1 diabetic children and their association with beta-pancreatic autoantibodies

Type 1 diabetes is an organ specific autoimmune disease whose incidence is increasing worldwide. A functional imbalance in cytokine production resulting in dominance of T helper (Th1) over Th2-type response has been suggested to play a critical role in the pathogenesis of type 1 diabetes. To measure serum concentrations of interleukin (IL)-1beta, IL-2 and IL-4 in children with recently diagnosed type 1 diabetes and to evaluate the autoimmune response measuring glutamic acid decarboxylase (GAD65) and tyrosine phosphatase like (IA-2) autoantibodies. 120 diabetic children and 118 age and gender matched control children, were recruited for this study. Circulating levels of IL-1beta IL-2 and IL-4 were measured by ELISA. GAD65 and IA-2 were measured by RIA. Circulating levels of IL-1beta were elevated in type 1 diabetic children as compared to the control group (9.3 +/- 7.3 and 4.9 +/- 3.8 pg/ml respectively, p=0.01). Serum concentration of IL-2 was also higher in diabetic patients (19.8 +/- 13.1 and 113 +/- 9.1 pg/ml respectively, p=0.01). No differences in serum IL-4 were observed between diabetics and control. Diabetic children with one or two positive autoantibodies (IA-2 and/or GAD65) had significantly higher levels of IL-1beta and IL-2 and lower levels of IL-4 than diabetic children without positive autoantibodies. High concentrations of IL-1beta were associated with an early onset of the disease. High levels of IL-1beta and IL-2 were found in diabetic children with recent diagnosis of the disease. Diabetics with positive antibodies against GAD65 and IA-2 had higher levels of IL-1beta and IL-2 and lower levels of IL-4 than their counterparts without positive antibodies.

Circulating levels of IL-1beta, a prothrombotic cytokine, are elevated in unstable angina versus stable angina.

Multiple studies support a role for inflammation in the pathogenesis of coronary atherosclerosis and unstable cardiac syndromes. However, of the known proinflammatory cytokines, only elevated plasma levels of interleukin-6 have been linked to unstable angina. We sought to examine the plasma levels of other major proinflammatory cytokines in similar clinical settings and to determine the extent of the relationship between inflammation and unstable coronary syndromes by measuring the levels of various proinflammatory cytokines in patients with stable and unstable angina. We measured plasma levels of interleukin-1 beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) in 97 patients: 67 with stable angina, 24 with unstable angina, and 15 healthy controls. Mean levels of IL-1beta were significantly higher in patients with unstable angina as compared to patients with stable angina (p =.009). Levels of IL-6 were significantly higher than control patients for both stable angina and unstable angina patients (p =.031 and.006, respectively). No significant differences were found in the levels of TNF-alpha. Our results suggest that both IL-1beta and IL-6 contribute to the pathogenesis of unstable angina, and that the profile of circulating plasma levels of proinflammatory cytokines differs in unstable angina from that in stable angina. Abbreviated Abstract. Multiple studies support a role for inflammation in the pathogenesis of coronary atherosclerosis and unstable cardiac syndromes. We measured plasma levels of interleukin-1 beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha), and interleukin 6 (IL-6) in patients with stable and unstable coronary syndromes. Levels of IL-1beta and IL-6 were found to be elevated in patients with unstable coronary syndromes. No significant differences were found in the levels of TNF-alpha. Our results suggest that both IL-1beta and IL-6 contribute to the pathogenesis of unstable angina.

Pilot evaluation of cytokine levels in patients undergoing radiotherapy for brain tumor.

This study was undertaken to evaluate plasma levels of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha) transforming growth factor-beta (TGF-beta), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF) in 3 pediatric and 14 adult patients receiving radiotherapy for brain tumor. Patients with glioblastoma, astrocytoma, chondrosarcoma, meningioma, schwannoma, and lung adenocarcinoma that had metastasized to the brain were included. Peripheral blood samples were collected before and after treatment with conventional photon and/or proton radiation; samples from healthy volunteers served as controls. Enzyme-linked immunosorbent assays were performed to quantitate the cytokines. Before irradiation, most patients had greater amounts of one or more of the cytokines compared with the mean obtained for control plasma. This was especially striking in patients with chondrosarcoma; the mean values for TGF-beta 1, TNF-alpha, bFGF, and EGF were 1458, 1289, 332, and 92% higher than in healthy subjects, respectively. After irradiation, bFGF and total TGF-beta 1 decreased in the majority of tested subjects. In contrast, IL-1 beta was detected only in pediatric patients (all with astrocytoma) and its levels after radiation were 33 to 67% higher than at pretreatment. EGF was found in four patients; post-treatment values were 125 to 608% higher in three of the individuals. These data show that cytokines are present at elevated concentrations in the blood circulation of patients with certain types of brain tumors and that changes in their levels can be detected after radiotherapy. Further investigations are warranted to determine whether these findings contribute to morbidity or therapeutic outcome.

Acute inflammatory reaction associated with endoluminal bypass grafts.

Nonspecific inflammatory reactions characterized by local tenderness, fever, and flu-like discomfort have been seen in patients undergoing endoluminal graft placement in the abdominal aorta or the femoral arteries. We undertook a study to assess the clinical and laboratory parameters of this inflammation. Ten patients with femoropopliteal artery (n = 9) or aortic (n = 1) lesions were treated with EndoPro System 1 stent-grafts made of nitinol alloy and covered with a polyester (Dacron) fabric. Eleven patients implanted with a bare nitinol stent served as the control group. In the stent-graft group, four patients showed clinical signs of acute inflammation manifested by fever and local tenderness. Three of these patients suffered thrombosis of the stent-grafts during the first month of follow-up. Plasma levels of interleukin-1 beta and interleukin-6 in all stent-graft patients were markedly increased 1 day after intervention (7.3 +/- 2.8 versus 90.2 +/- 34.1 pg/mL and 15.6 +/- 5.8 versus 175.5 +/- 66.3 pg/mL, respectively; p < 0.01). This was followed by an increase in fibrinogen (3.0 +/- 0.2 versus 5.0 +/- 0.2 g/L; p < 0.05) and C-reactive protein (14.6 +/- 3.3 versus 77.5 +/- 15.0 mg/L; p < 0.01) at 1 week. No direct correlation between the inflammatory markers and symptoms could be found. In vitro analysis showed that individual components of the stent-graft did not activate human neutrophils, whereas the intact stent-graft itself induced a marked neutrophil activation. The component of the self-expanding stent-graft responsible for the nonspecific inflammatory reaction was not identified in this study. It is likely that the stent-graft itself or some as yet unrecognized element of the device other than the Dacron fabric or metal alloy may be a potent in vivo inducer of cytokine reaction by neutrophils.

Influence of Hemodialysis Membranes on Gene Expression and Plasma Levels of Interleukin‐iβ

Plasma levels of interleukin-1 beta (IL-1 beta) were measured in 10 normal subjects, in 11 nondialyzed end-stage renal failure (ESRD) patients, and in 22 hemodialysis (HD) patients. Of the HD patients, 7 were dialyzed with Cuprophan (CU), 7 with polymethylmethacrylate (PMMA), and 8 with polysulphone (PS) dialyzers. In normal controls, nondialyzed ESRD patients, and HD equipped with CU, PAMM, and PS dialyzers, plasma levels of IL-1 beta were 10.73 +/- 5.24 pg/ml, 9.97 +/- 3.61 pg/ml, 13.17 +/- 4.04 pg/ml, 15.16 +/- 6.16 pg/ml, and 13.96 +/- 5.47 pg/ml, respectively. There were no statistically significant differences among the groups (p > or = 0.05). In contrast, the gene expression of IL-1 beta for peripheral blood mononuclear cells (PBMC) by in situ hybridization showed differences among the groups. The gene for IL-1 beta for PBMC appears in HD equipped with different membranes, but not in cases of nondialyzed uremic patients and normal subjects. With computer imaging analysis, we carried out quantitative analysis of cells in in situ hybridization with an area of positive spots to an area of total cells. In HD with CU, PMMA, and PS, the results were 10.64 +/- 1.07, 3.34 +/- 0.74, and 3.27 +/- 0.64%, respectively. The levels of IL-1 beta gene expression in CU were higher than that in PMMA or PS. There were statistically significant differences (p < or = 0.001) between CU and PMMA or PS and no significant difference between the PMMA and PS (p > or = 0.05). We suggest measuring the gene expression of cytokines for PBMC and which may be better than measuring cytokine levels only for investigating the blood compatibility of dialyzers, which may help in understanding chronic complications of the dialysis procedure.

Plasma levels of IL-1β, TNFα and their specific inhibitors in undialyzed chronic renal failure, CAPD and hemodialysis patients

The presence of naturally occurring inhibitors of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in a variety of diseases has been demonstrated. The IL-1 receptor antagonist (IL-1Ra) binds to IL-1 receptors and blocks the activity of IL-1, and a soluble form of the p55 TNF receptor (TNFsRp55) binds and neutralizes TNF. In the present study, plasma levels of IL-1 beta, IL-1Ra, TNF alpha and TNFsRp55 were measured in 29 undialyzed patients with chronic renal failure (CRF), 13 patients on continuous ambulatory peritoneal dialysis (CAPD), 42 patients on chronic hemodialysis (HD) and in 15 healthy controls. Of the 29 patients with CRF, 13 had end-stage renal disease (ESRD, estimated GFR < 10 ml/min). Among health controls, plasma levels of IL-1 beta, IL-1Ra and TNF alpha were at or below the limit of detection of the assay. In undialyzed patients with ESRD, or in patients on CAPD or HD, plasma levels of IL-1 beta were 428 +/- 134 pg/ml, 378 +/- 83 and 352 +/- 43 pg/ml, respectively. Although plasma levels of IL-1 beta in each group of patients were higher than those in healthy controls (< 160 pg/ml), these differences were not statistically significant. In contrast, plasma levels of IL-1Ra in undialyzed patients with ESRD (629 +/- 125 pg/ml, P = 0.03), CAPD (902 +/- 164 pg/ml, P < 0.0001) and HD patients (642 +/- 73 pg/ml, P = 0.004) were significantly higher than those in healthy controls (103 +/- 15).(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma cytokines following thermal injury and their relationship with patient mortality, burn size, and time postburn.

We measured plasma levels of interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha), and interleukin-6 (IL-6) following thermal injury. Cytokine levels in the plasma of 27 burned patients were serially screened by ELISA and compared with cytokine levels in 16 healthy laboratory employees. The relationships between cytokine concentrations and patient mortality, burn size, and time postburn were examined. Plasma samples with detectable amounts of IL-1 beta and IL-6 were significantly more frequent in burned patients than in controls, whereas TNF alpha was undetectable in most plasma samples. All nonsurviving burned patients had detectable IL-6 levels; these were significantly higher than those of surviving patients. The IL-1 beta and IL-6 concentrations were highest during the first week after injury and declined over time. The IL-1 beta concentrations were positively correlated with burn size. These findings suggest that IL-1 beta and IL-6 may influence metabolic and immunologic responses in the first few weeks following thermal injury. Tumor necrosis factor alpha was transiently elevated in a small subpopulation of burned patients with no obvious relationship to burn size or time postburn.