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)

Renal vasculitis syndromes include particular characteristic changes in concentrations of some cytokines in plasma or urine. Preliminary results suggest that the systemic lupus erythematodes with affliction of the kidneys is specifically concomitted by the increase in IL-8, both in plasma and urine. ANCA-positive renal vasculitis syndromes appear to coincide with a typical increase in the synthesis of interleukin-6 in the kidneys. We suggest that the monitoring of individual cytokine levels in plasma and urine will enable to study in greater detail the immunopathogenesis of renal vasculitis syndromes and the extent of local production of cytokines which may cause further progression of renal lesions. (Fig. 4, Tab. 1, Ref. 10.).
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PMID:[Adhesion molecules and cytokines in vasculitides]. 862 Mar 22

The pathogenetic mechanism of vasculitis in systemic lupus erythematosus (SLE) remains a subject of debate. Evidence for a direct pathogenetic role of anti-double-stranded DNA antibodies (anti-dsDNA) is not strong. Supernatant concentrations of interleukin-1 beta and interleukin-6, and mRNAs encoding for interleukin-1 alpha and interleukin-1 receptor-1 were determined in cultured human umbilical vein endothelial cells (HUVEC), incubated with control IgG (n = 18), anti-dsDNA (n = 18), or IgG from the same lupus patient depleted of anti-dsDNA by affinity chromatography (anti-dsDNA-dep-IgG). Compared with control IgG, there was a significant increase of supernatant interleukin-1 beta and interleukin-1 alpha mRNA in endothelial cells incubated with anti-dsDNA. The supernatant interleukin-1 beta and interleukin-6, and mRNAs encoding for interleukin-1 alpha and interleukin-1 receptor-1, were significantly elevated in endothelial cells incubated with anti-dsDNA, compared with those incubated with anti-dsDNA-dep-IgG. Pretreating HUVEC with native DNA before incubating with anti-dsDNA did not result in an additive effect. These in vitro studies suggest that anti-dsDNA plays an important pathogenetic role in inducing inflammatory injury of vascular endothelium in SLE.
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PMID:Anti-DNA autoantibodies stimulate the release of interleukin-1 and interleukin-6 from endothelial cells. 869 26

Systemic lupus erthematosus (SLE) has been very often associated with complication in reproduction. 29 SLE women divided into two groups A (10 patients aged 18-36 years) and B (19 patients aged 42-67 years) were queried with regard to general, obstetric and SLE history by the use of a questionnaire. Serum of each patient was tested for interleukin-6 (by ELISA), sperm antibodies (by mixed antiglobulin reaction and tray agglutination test) and zona pellucida antibodies (passive haemagglutination test and ELISA methods). Neuropathic, cutaneous and nephrotic symptoms prevailed in the SLE women. The group of younger women showed significant problems in fertility (only one woman became a happy mother) while 15 women in the elderly group were successfully pregnant before SLE diagnosis. Low serum II-6 levels were detectable only in 3 cases as a possible consequence of corticoid treatment. Levels of zona pellucida antibodies were higher in the elderly group B, levels of sperm antibodies were higher in contrast to younger SLE women (group A). The laboratory findings may be related to the severity of autoimmune disease and to menopause onset (group B) or good sexual activity (group A).
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PMID:Systemic lupus erythematosus in women and serum interleukin-6, sperm and zona pellucida antibodies. 876 1

Cytokines are believed to play an important role in the pathogenesis of systemic lupus erythematosus (SLE). However, for tumour necrosis factor alpha (TNF-alpha) both beneficial and deleterious effects have been reported. To obtain information about the involvement of this cytokine in the pathophysiology of SLE, serum levels of TNF-alpha, the soluble forms of the 55 and 75 kDa tumour necrosis factor receptors (TNF-R55 and TNF-R75), and interleukin-6 (IL-6) were measured by ELISA in nine female patients over a period of 2 yr. Compared to healthy controls, levels of TNF-alpha (median 47 pg/ml, range < 15-222 pg/ml), TNF-R55 (median 1.9 ng/ml, range 0.8-10.8 ng/ml), TNF-R75 (median 4.7 ng/ml, range 1.5-15 ng/ml) and IL-6 (median 3.5 pg/ml, range < 3.5-52 pg/ml) were significantly elevated in SLE patients (P < 0.0001 vs controls in all cases). There were strong correlations between TNF-alpha and its soluble receptors (P < 0.0001). Moreover, TNF-alpha and both TNF-Rs strongly correlated with clinical and serological parameters of disease activity, such as the European Consensus Lupus Activity Measurement (ECLAM) score, anti-dsDNA antibodies, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and anaemia (P < 0.0001 for all comparisons). TNF-alpha and TNF-R75 also correlated with IL-6 (P < 0.0001). However, no correlation between IL-6 and ECLAM was found, and the correlation of IL-6 with anti-dsDNA was relatively weak; in contrast, IL-6 correlated strongly with CRP and ESR (P < 0.0001). Although these data do not allow us ultimately to discriminate between beneficial and deleterious effects of TNF-alpha, they nevertheless suggest a central role for the TNF system in the pathophysiology of SLE.
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PMID:Tumour necrosis factor alpha and its soluble receptors parallel clinical disease and autoimmune activity in systemic lupus erythematosus. 894 91

It has been previously reported that the production of interleukin-6 (IL-6) is often enhanced in systemic lupus erythematosus (SLE). The authors examined the secretion of IL-6, tumour necrosis factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor, IL-1 alpha and IL-4 by B cells and monocytes from lupus patients and compared this to the production in normal controls and in rheumatoid arthritis patients. IL-6 production was increased an average of 3.4-fold compared to that in normal subjects and 8.4-fold compared to rheumatoid arthritis patients. In SLE, a strongly positive correlation was found between the levels of IL-6 and TNF-alpha (R = 0.8987, P = 0.002). Since production of both IL-6 and TNF-alpha is regulated by IL-10, the enhancement of the production of these cytokines could reflect a defect in either IL-10 production or responsiveness. However, spontaneous production of IL-10 was enhanced in cultures of B cells and monocytes from lupus patients, compared to normal controls, the levels being increased 3.1- to 6-fold for monocytes and B cells, respectively. The finding of increased secretion of these cytokines implies an abnormality in IL-10-mediated suppression in SLE. To assess this possibility, the authors examined recombinant human IL-10-mediated suppression of IL-6 production by monocytes and B cells from lupus patients, compared to normal controls, and found that whereas IL-10 caused a concentration-dependent suppression of IL-6 production in normal B cells and monocytes, this suppression was deficient in B cells and monocytes from lupus patients. In SLE, it therefore appears that there may be an intrinsic defect in IL-10-induced suppression of cytokine synthesis. This could explain the increased levels of IL-10 and IL-6 found in this condition, and may also be responsible for the characteristic polyclonal B-cell activation that is seen.
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PMID:Interleukin-10 response abnormalities in systemic lupus erythematosus. 935 Feb 93

Because of the high morbidity and mortality in patients with bacterial arthritis, rapidly and correctly diagnosing this critical condition is a challenge to emergency clinicians. Synovial fluid samples were obtained from 75 patients with arthritis disorders who presented to an emergency service, and levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) were measured. Twenty patients with culture-proven bacterial arthritis had higher levels of synovial TNF-alpha than patients with osteoarthritis or with inflammatory arthritis, including gouty arthritis, rheumatoid arthritis, reactive arthritis, and lupus arthritis. There was a good sensitivity for synovial TNF-alpha level in diagnosing patients with bacterial arthritis. Nearly 100% of patients with bacterial arthritis had elevated synovial TNF-alpha levels. However, synovial IL-1 beta and IL-6 levels failed to discriminate bacterial arthritis from other inflammatory arthritis. Measurement of synovial TNF-alpha level may be useful as a diagnostic aid in emergency patients with bacterial arthritis disorders.
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PMID:Measurement of synovial tumor necrosis factor-alpha in diagnosing emergency patients with bacterial arthritis. 937 40

We investigated the levels of prolactin (PRL) and interleukin-6 (IL-6) in the cerebrospinal fluid (CSF) and serum of systemic lupus erythematosus patients with central nervous system involvement (CNS-SLE), and examined whether PRL and IL-6 have a relationship. Serum and CSF PRL and IL-6 were measured in the following groups of patients and controls: group I: seven patients with CNS-SLE; group II: three SLE patients without CNS involvement (non CNS-SLE); group III: 10 patients with neurocysticercosis; and group IV: six healthy women. The patients were clinically assessed. CSF PRL and IL-6 were elevated in group I (CNS-SLE) in comparison with all other groups (p<0.001). In addition, four of seven patients had higher levels of IL-6 and PRL in CSF than in serum. A positive correlation between PRL and IL-6 in CSF of SLE was observed (r=0.88, p<0.001). The mean serum PRL concentrations were not significantly different in all groups, but high levels of IL-6 were found in the serum of group I in comparison with groups II and IV (p<0.001). The serum levels of group III were not different from those of group I. These results demonstrate the presence of intrathecal synthesis and elevations of CSF PRL and IL-6 in active CNS-SLE involvement and indicate that measurements of CSF PRL and IL-6 may be useful in the evaluation of neuropsychiatric lupus erythematosus.
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PMID:Prolactin and interleukin-6 in neuropsychiatric lupus erythematosus. 964 6

We report here a case of neuropsychiatric lupus erythematosus with organic brain syndrome and transverse myelitis which was successfully managed by plasmapheresis. A 27-year-old female with facial rash, arthralgia and fever was diagnosed as having SLE and treated with oral prednisolone (PSL) in June 1996. After 6 weeks she demonstrated muscle pain and a spiking temperature. The dose of PSL was increased but clinical symptoms did not improve. In August, pulse methyl-PSL was performed and she subsequently-developed delirium, impairment of orientation, memory and perception, which were followed by paraplegia of the lower extremities and loss of sphincter control. Intravenous bolus cyclophosphamide was not effective, but liver dysfunction, bone marrow suppression and respiratory failure due to an infection of pneumocystis carinii were observed. We then performed plasmapheresis or immunoabsorption several times. After this treatment steady improvement was observed. High values of antiribosomal P protein antibodies in the serum and interleukin-6 in the cerebrospinal fluid decreased. Small foci of increased signal intensity detected on cranial magnetic resonance imaging and hypoperfused areas on single-photon emission CT diminished. The patient was maintained on low-dose PSL and no recurrence has been observed 15 months from the onset.
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PMID:[A case of severe neuropsychiatric lupus erythematosus treated by plasmapheresis: diagnostic values of serum antiribosomal P protein antibodies and interleukin-6 in cerebrospinal fluid]. 979 79

The psychiatric and cognitive condition of a patient with lupus psychosis was evaluated. Using a device that detects the corneal reflection of infrared light, the patterns of eye tracking movements were recorded before the onset of lupus psychosis, after remission, and again 1 year later. Electroencephalographic findings and cerebrospinal fluid levels of both interferon alpha and interleukin-6 were also obtained longitudinally. Electroencephalographic findings and clinical signs were correlated to the levels of interferon alpha in cerebrospinal fluid. Analysis of exploratory eye movements revealed marked decreases in the number of eye fixation, mean eye-scanning length and total eye-scanning length. Even though the lupus psychosis resolved and the electroencephalographic findings became normal, the eye movement patterns showed remaining deterioration. It was concluded that analysis of exploratory eye movements in patients with systemic lupus erythematosus may be useful in diagnosing lupus psychosis, and may also present a diagnostic clue to subclinical lupus psychosis.
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PMID:Analysis of exploratory eye movement in a patient with lupus psychosis. 980 82

Anti-CD4 antibodies have been recently introduced into the therapy of various autoimmune diseases, among them systemic lupus erythematosus (SLE). Their modes of action are not yet fully understood. Interference with cytokine release may be one possible mechanism. Therefore, the effects of anti-CD4 antibodies on the cytokine release of IL-6 (interleukin-6) and TNF-alpha (tumor necrosis factor alpha) were investigated in a whole blood culture system. Basal and phytohemagglutin/lipopolysaccharide (PHA/LPS)-stimulated cytokine patterns were compared to cytokine release after the addition of anti-CD4 antibodies (MAX.16H5) or methylprednisolone in short time whole blood cell culture systems from 12 patients with active SLE, 23 patients with inactive SLE and 12 healthy volunteers. TNF-alpha and IL-6 concentrations were determined in the supernatants by ELISA. High disease activity correlated with an increased production of proinflammatory cytokines. Cell cultures of patients with inactive SLE showed a diminished capacity to respond to mitogenic stimulation. Anti-CD4 antibodies added in vitro suppressed significantly the unstimulated production of IL-6 (P<0.02) in the cell cultures of patients with active SLE and in the PHA/LPS-stimulated cell cultures from both groups of SLE patients (both P<0.001) and healthy volunteers (P<0.01). However, MAX.16H5 did not affect the release of TNF-alpha. In control samples methylprednisolone considerably reduced stimulated and unstimulated IL-6 and TNF-alpha production in all SLE patients, irrespective of the disease state, and in all healthy controls. These data indicate that the proinflammatory cytokines are involved in the pathogenesis of SLE. It is assumed that anti-CD4 antibodies, which can be effective in the treatment of highly active lupus patients, may act via their influence on cytokine release. The decrease of the proinflammatory cytokines IL-6 under therapy with MAX.16H5 could explain the observations of clinical trials and animal studies which showed a reduction of inflammatory parameters and diminished production of autoantibodies following treatment with anti-CD4 antibodies.
Lupus 1999
PMID:Effects of anti-CD4 antibodies on the release of IL-6 and TNF-alpha in whole blood samples from patients with systemic lupus erythematosus. 1060 44


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