Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytokines at an inflammatory site may be a better indicator of the clinical severity of an infectious disease than the serum levels of the cytokines. Concentrations of interleukin-1 beta (IL-1 beta) in paired samples of cerebrospinal fluid (CSF) from 10 rabbits with experimental bacterial meningitis caused by H. influenzae type b, were measured, and compared to the concentrations of four cytokines; IL-1 beta, interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) in CSF samples from 45 children with or without meningitis. The IL-1 beta concentrations in the CSF from rabbits with experimental meningitis were significantly higher than the concentrations in control animals without meningitis (p < 0.001). The mean CSF concentrations of IL-8 from meningitic children were significantly higher than in the control group without meningitis (p < 0.005). TNF-alpha was only detected in septic meningitis. Assays of IL-6, however, were not significantly different in the septic meningitis group, the aseptic meningitis group and the non-meningitis group. These data indicate a possible role of IL-1 beta, IL-8 and TNF-alpha as mediators in the meningeal inflammatory process in patients with meningitis and TNF-alpha, in particular, may play a role in the pathogenesis of septic meningitis.
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PMID:Concentrations of interleukin-1 beta, interleukin-6, interleukin-8 and TNF-alpha in cerebrospinal fluid from children with septic or aseptic meningitis. 130 8

Group B streptococci (GBS) are a leading cause of sepsis and meningitis in neonates. Since cytokines are thought to play an important role in septic shock, we have studied serum levels of tumor necrosis factor-alpha (TNF alpha) and interleukin-6 (IL-6) in BALB/c mice infected with type III GBS. TNF alpha and IL-6 were detected by the L929 cytotoxicity and the B9 proliferation assays, respectively, in serial serum samples obtained after infection. After i.p. challenge with an LD50, serum TNF alpha rose above baseline values as early as 3 hr, peaked at 7 hr, and returned to baseline values at 20 hr. IL-6 serum levels rose concomitantly with TNF alpha, peaking 8 hr after challenge. No serum TNF alpha activity was detected in the course of sublethal infections. However, a transient rise in TNF alpha levels was observed after i.v. inoculation of high numbers (greater than or equal to 1 x 10(8) of heat-killed GBS. When groups of mice were injected i.v. with a single dose of anti-TNF alpha rabbit serum 2 hr before challenge with an LD90 or LD30, no effect was noted in terms of survival, although the serum TNF alpha peak was completely abrogated. Serum TNF alpha does not seem to play an obligatory role in GBS-induced lethality of adult mice. However, further studies are needed to assess better the role of this cytokine in the pathogenesis of GBS sepsis.
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PMID:Production of tumor necrosis factor-alpha and interleukin-6 in mice infected with group B streptococci. 142 22

Interleukin-6 (IL-6) is multipotent cytokine that acts in a network of factors directing the inflammatory reaction of purulent bacterial meningitis (PBM). However, little is known about the role of IL-6 in aseptic or "viral" meningitis (AM). IL-6 was assayed by RIA in cerebrospinal fluid (CSF) and serum samples obtained from patients with AM (n = 65), PBM (n = 8), and lymphocytic bacterial meningitis (LBM, n = 11). Of patients with AM, 89% had detectable IL-6 in CSF, with high IL-6 titers (median, 2160 pg/mL; 95% confidence interval [CI], 1320-2540 pg/mL) compared with 100% in patients with PBM (median, 6575 pg/mL; 95% CI, 450-32,000 pg/mL) and 90.9% in patients with LBM (median, 875 pg/mL; 95% CI, 150-2180 pg/mL). There was a highly symmetrical correlation between IL-6 and the percentage of polymorphonuclear cells in CSF of patients with PBM (r = .97, P = .01) and AM (r = .49, P = .002). In conclusion, this study shows evidence that IL-6 is released into the meningeal space in aseptic meningitis and is correlated with the local acute inflammatory response.
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PMID:High concentrations of intrathecal interleukin-6 in human bacterial and nonbacterial meningitis. 163 15

We present a double-antibody radioimmunoassay for determining human interleukin-6 (IL-6) in biological fluids. The detection limit of the assay is 20 ng/L (B0 - 2 SD). Bound radioactivity in the range of 30% to 90% of the B0 counts corresponds to IL-6 concentrations of 100 to 14,000 ng/L. Analytical recovery of IL-6 added to EDTA-treated plasma averaged 25% more than that added to serum. The plasma concentration of IL-6 was therefore approximately 85 ng/L more than the concentration in simultaneously drawn serum. The mean serum concentration of IL-6 in 45 healthy subjects was 83 ng/L (range 20-290 ng/L), in 20 patients with multiple myeloma 303 ng/L, in 20 patients with rheumatoid arthritis 234 ng/L, and in 13 patients with systemic lupus erythematosus 183 ng/L. Markedly increased (greater than 3000 ng/L) concentrations of IL-6 were found in sera of patients with meningococcus meningitis and infectious peritonitis.
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PMID:Radioimmunoassay of interleukin-6 in plasma. 191 67

We examined the measurement and the diagnostic value of cerebrospinal fluid interleukin-6 (CSF IL-6) in meningitis. The cytokine was measured by bioassay (B9 hybridoma cell line) and by immunoassay (in-house radioimmunoassay). We compared the diagnostic value of CSF IL-6 determination with that of other biochemical markers of meningitis. Although there was significant correlation between bioactive and immunoactive IL-6 (r = 0.724, P < 0.001), results were frequently different with biological/immunological ratios ranging from 0.2 to 24.3 (mean 4.6). Gel permeation chromatography suggested that the discrepancy in biological and immunological activities was not due to molecular heterogeneity, but may be explained by the presence of a synergistic factor. Interleukin-6 concentration was markedly elevated in CSF from most patients with bacterial meningitis compared to patients with viral meningitis and those without evidence of infection. However, low IL-6 levels by radioimmunoassay did not exclude bacterial meningitis (sensitivity 86%). CSF total protein and CSF glucose were significantly different between all three groups, but there was no significant difference in lactate concentration between virally infected and normal CSF, both of which had lower lactate concentrations than those in bacterial infection. CSF IL-6 measurement had greater sensitivity, specificity and predictive value than these other biochemical markers, and hence a rapid assay for IL-6 in CSF may contribute to the early diagnosis of bacterial infection.
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PMID:Cerebrospinal fluid interleukin-6 and its diagnostic value in the investigation of meningitis. 763 33

We sought to determine whether the detection of cytokines, produced during the inflammatory response, would aid in the diagnosis of meningitis in young infants. We measured cerebrospinal fluid (CSF) and plasma levels of interleukin-6 (IL-6) and tumor necrosis factor (TNF) in 62 infants less than 6 months of age whose condition was evaluated for meningitis. Twenty infants had culture-proved meningitis, 22 had aseptic meningitis, and 20 control infants had no evidence of meningitis. The CSF IL-6 levels were elevated in all 20 infants with bacterial meningitis and in 9 of 22 infants with aseptic meningitis but were undetectable in all control subjects. Furthermore, CSF IL-6 levels were 10 times greater in infants with bacterial versus aseptic meningitis (p < 0.001). Levels of TNF in CSF were detected in 12 of 20 infants with bacterial meningitis and were undetectable in infants with aseptic meningitis and in control infants (p < 0.02). Plasma IL-6 and TNF levels were unreliable for the detection of meningitis in this patient population. We conclude that the presence of IL-6 in the CSF reliably identifies infants with meningitis and that the presence of CSF TNF is a highly specific indicator of bacterial meningeal inflammation.
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PMID:Cytokine elevations in infants with bacterial and aseptic meningitis. 777 86

This study investigated whether the 21-aminosteroid U74389F, an inhibitor of lipid peroxidation, attenuates pathophysiologic changes in experimental pneumococcal meningitis. Infected rats injected intravenously with vehicle of [corrected] U74389F developed increases in regional cerebral blood flow (rCBF), intracranial pressure (ICP), brain water content, and white blood cells (WBC) in cerebrospinal fluid (CSF) within 8 h after intracisternal challenge. Pretreatment with or administration of U74389F 4 h after infection significantly reduced the increase in ICP but had no effect on rCBF increase. Moreover, U74389F pretreatment significantly reduced brain water content and CSF WBC count. In vitro, U74389F inhibited iron-dependent lipid peroxidation of astrocyte cultures and the production of tumor necrosis factor-alpha, interleukin-6, and nitric oxide by stimulated macrophages. These data suggest that U74389F modulates early pathophysiologic alterations in experimental pneumococcal meningitis.
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PMID:Protective effect of a 21-aminosteroid during experimental pneumococcal meningitis. 779

The mechanism underlying meningitis-associated brain injury is unclear. This study investigated the hypothesis that lipopolysaccharide (LPS) alters astrocyte function and structure via the release of proinflammatory cytokines. In enriched murine astrocyte cultures, LPS inhibited (P < 0.05) glutamine synthetase activity, 3H-gamma aminobutyric acid uptake, and DNA synthesis; LPS also induced ultrastructural changes. Antibodies to tumor necrosis factor-alpha, interleukin-1, and interleukin-6 blocked (P < 0.05) in part the LPS-induced inhibition of astrocyte function. Also, treatment of astrocyte cultures with cytokines significantly altered these astrocyte functions and ultrastructure. Taken together, the present findings support the hypothesis that LPS affects astrocyte function and structure via the release of proinflammatory cytokines, especially tumor necrosis factor-alpha.
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PMID:Role of cytokines in lipopolysaccharide-induced functional and structural abnormalities of astrocytes. 791 Aug 8

Concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) in cerebrospinal (CSF) samples were determined from 11 control and 42 children with central nervous system infections including 11 patients with bacterial meningitis, 20 patients with aseptic meningitis, 11 patients with encephalitis. The CSF IL-6, IL-8 and TNF-alpha concentrations in patients with bacterial meningitis were significantly higher than those with aseptic meningitis, encephalitis and the control groups. CSF IL-6, IL-8 and TNF-alpha levels in patients with aseptic meningitis were also significantly higher than those in the control group. There was no significant increase of CSF IL-6, IL-8 and TNF-alpha concentrations in patients with encephalitis compared to the control group. CSF IL-6 and TNF-alpha concentrations were decreased in patients with bacterial meningitis after treatment. CSF IL-8 levels were significantly decreased in both bacterial and aseptic meningitis groups at recovery period. There were no correlation between CSF IL-6, IL-8 and TNF-alpha levels and other parameters including CSF leukocytes, protein, sugar, IgG levels and IgG indexes in patients with bacterial meningitis. These results suggest that IL-6, IL-8 and TNF-alpha are important mediators in the meningeal inflammatory process in patients with meningitis. The levels of these mediators are good indicators for the extent of the meningeal inflammation.
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PMID:Cerebrospinal fluid interleukin-6, interleukin-8, and tumor necrosis factor-alpha in children with central nervous system infections. 893 5

Cytokines may play an important role in the pathophysiology of traumatic brain injury (TBI) in children. Interleukin-6 (IL-6) is a proinflammatory cyotkine that plays a role in regenerative processes within the central nervous system (CNS), whereas interleukin-10 (IL-10) is an antiinflammatory cytokine. Both have been measured in serum and cerebrospinal fluid (CSF) as an index of the degree of inflammation in diseases, including sepsis and meningitis. We hypothesized that both IL-6 and IL-10 would be increased in the CSF of children after severe TBI. Fifteen children who sustained severe TBI (Glascow Coma Score [GCS] < or = 7) were studied. Standard neurointensive care was provided. Ventricular CSF collected the first 3 days after TBI was analyzed for IL-6 and IL-10 concentrations by ELISA. Controls were 20 children who were evaluated for meningitis with diagnostic lumbar puncture subsequently found to have no CSF pleocytosis and negative cultures. IL-6 was increased in children after TBI versus controls on all days studied (day 1, 3158.2 +/- 621.8 pg/ml; day 2, 1111.6 +/- 337.0 pg/ml; day 3, 826.7 +/- 193.5 pg/ml vs. 20.6 +/- 5.8 pg/ml, p < 0.0001, Mann-Whitney Rank Sum). IL-10 was increased in children after TBI vs controls on all days studied (day 1, 47.2 +/- 12.9 pg/ml; day 2, 21.0 +/- 6.7 pg/ml; day 3, 15.5 +/- 5.9 pg/ml vs. 8.9 +/- 7.5 pg/ml, p < 0.01). Increased IL-10 concentrations were independently associated with age < 4 years and mortality (p = 0.004 and 0.04, respectively, multivariate linear model). This study demonstrates that IL-6 is increased after TBI in children to levels similar to those reported in adults and is the first to show that IL-10 is increased in CSF of humans after TBI. These data suggest that there may be an age-dependent production of IL-10 after TBI in children.
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PMID:Interleukin-6 and interleukin-10 in cerebrospinal fluid after severe traumatic brain injury in children. 925 63


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