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)

Systemic vasculitis is an inflammatory disorder of blood vessels characterized by a perivascular mononuclear cell infiltration around the vessel and fibrinoid necrosis within vessel walls. Interleukin-1 (IL-1) is a multipotent inflammatory mediator and affects several properties of vascular cells. To determine whether IL-1 could contribute to the pathogenesis of vascular diseases, we examined the effect of IL-1 on B cell stimulatory factor-2/interleukin-6 (IL-6) production by cultured human vascular smooth muscle cells (SMC) and the proliferation of these cells. Supernatants of SMC stimulated IgM synthesis of human B cell line. SKW6-CL4 cells. This activity was increased (1.7 to 2.6-fold) when SMC were pretreated with IL-1 or calcium ionophore A23187 for 48 h, and was completely blocked by rabbit anti-human IL-6 antibodies. These IL-6 activities of the SMC supernatants were also assessed by using an IL-6 dependent murine hybridoma cell line. MH-60. BSF-2. In addition, we observed that pretreatment of SMC with IL-1 for 48 h stimulated growth of SMC during the 96 h incubations, as assessed by cell number (p less than 0.05). These results suggest that IL-1 may contribute to the pathogenesis of inflammatory and immunological vasculitis by the augmentation of IL-6 release and growth of SMC.
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PMID:Pretreatment of human vascular smooth muscle cells with interleukin-1 enhances interleukin-6 production and cell proliferation (action of IL-1 on vascular smooth muscle cells). 210 9

A 43-year-old woman with a 10-year history of bronchial asthma developed marked peripheral blood eosinophilia and symptoms of vasculitis. A diagnosis of Churg-Strauss syndrome (CSS) was made, and her symptoms were successfully treated with low-dose prednisolone. Serum rheumatoid factors (RF) of both IgG and IgM, but not IgA or IgE, subclasses transiently appeared in accordance with the vasculitic phase. Serum interleukin-6 (IL-6) levels also transiently increased in this phase and the peak level was reached just prior to the maximum of RF elevation, suggesting the role of IL-6 as an inducer of RF. RF and IL-6 seemed to be involved in the pathogenesis of the vasculitis in this patient.
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PMID:IgG and IgM rheumatoid factor levels parallel interleukin-6 during the vasculitic phase in a patient with Churg-Strauss syndrome. 749 76

Juvenile polyarteritis syndrome (JPS) is an idiopathic febrile disease in dogs. Elevated serum levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) have been reported in human patients with vasculitis. We investigated whether these cytokines are also elevated in serum of dogs with JPS using sensitive bioassays. Increased levels of IL-6 activity were detected in the serum of 12 acutely ill dogs, whereas the IL-6 activity decreased to low or undetectable levels during convalescence. Treatment of 5 acute JPS dogs with prednisone resulted in a rapid clinical improvement accompanied by a decrease of IL-6 activity. Withdrawal of prednisone treatment caused reappearance of clinical symptoms and high serum IL-6 activity within a few days. TNF activity could not be detected in the samples of normal dogs, convalescent JPS, or acute JPS dogs. These studies support a role for IL-6 in the pathogenesis of JPS.
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PMID:Interleukin-6 activity in dogs with juvenile polyarteritis syndrome: effect of corticosteroids. 755 74

This study was designed to investigate serum soluble interleukin-2 receptor (S-IL-2R), interleukin-2 (IL-2) and interleukin-6 levels (IL-6) in patients with either a positive or negative Borrelia burgdorferi serology. Serum samples from 101 individuals, divided in to five groups according to clinical symptoms and outcome of serology were analysed. Samples of cerebrospinal fluid (CSF) from nine of the individuals were also studied. The highest average serum S-IL-2R levels (1,180 +/- 1,140 U/ml) were found in patients with erythema migrans, the hallmark of Lyme borreliosis, followed by patients with symptoms closely related to Borrelia infection (900 +/- 1,200 U/ml) and with a strong positive serology. In two patients with central nervous system (CNS) involvement, increased levels of S-IL-2R of 920 and 620 U/ml respectively (normal value < 50 U/ml) were detected in the CSF. No statistically significant relationship between IgG or IgM antibody activity and serum S-IL-2R levels was found. Detectable levels of IL-2 were only found in three patients. Increased levels of IL-6 were found in sera from 14 patients. The highest concentration, 90 pg/ml (normal value < 10 pg/ml), was measured in a patient presenting with vasculitis. In conclusion, B. burgdorferi infection causes a moderate increase of serum S-IL-2R levels, although there is no relationship between the severity of the infection, as estimated by the antibody concentration or to serum IL-2 or IL-6 levels. Secondary complications of the infection, such as vasculitis, may cause an increased level of serum IL-6.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of soluble IL-2 receptor, interleukin-2 and interleukin-6 in patients with positive and negative Borrelia burgdorferi serology. 784 8

Alfa-1-antitrypsin (a-1-AT), C-reactive protein (CRP) and interleukin-6 (IL-6) serum levels were measured during different phases of anti-neutrophil cytoplasmic antibody (ANCA)-positive vasculitis. Correlation between ANCA and these variables was observed. Both a-1-AT and CRP fluctuations indicated changes in activity that could not always be detected by ANCA. On the other hand, these acute phase proteins were also less specific. IL-6 was not as sensitive as CRP and a-1-AT, a clearly increased mean value was observed only in patients with high ANCA titers.
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PMID:Alpha-1-antitrypsin, CRP and interleukin-6 in ANCA-positive vasculitis. 829 30

Plasma immunoreactive endothelin (iET) levels were investigated in patients with Kawasaki disease (KD). The iET level was 2.49 +/- 0.13 pg/mL in KD patients and 1.32 +/- 0.06 in age-matched control subjects, showing a significant increase with KD. The iET level was not increased in patients with febrile inflammatory diseases of bacterial origin without KD (non-KD group). Parameters indicating an inflammatory reaction, such as C-reactive protein, platelet count, white blood cell count, and interleukin-6 level, were increased in the KD patients. However, they were similarly increased in the patients with febrile diseases of bacterial origin and showed no significant differences between the two groups. This study is the first to report that plasma iET levels are elevated in a disease mainly involving vasculitis. These results suggest that blood iET levels are increased in KD patients as a result of the associated vascular endothelial damage and that iET can be a useful marker for the diagnosis of KD.
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PMID:Increased plasma endothelin levels in Kawasaki disease: a possible marker for Kawasaki disease. 835 99

The pathogenesis of central nervous system (CNS) involvement in vasculitides remains unclear. We evaluated cerebrospinal fluid (CSF) interleukin-6 (IL-6) activity in relation to the CNS disease activity in vasculitides. Three patients with vasculitides of different categories who showed CNS manifestations were studied, including polyarteritis nodosa, temporal arteritis, and Behcet's disease. All three patients showed marked elevation of CSF IL-6 activity in parallel with the CNS disease activity. In one of the three patients, cerebral vasculitis was demonstrated histologically. All these patients also showed elevation of serum IL-6 activity in parallel with systemic symptoms, such as fever and/or elevation of C-reactive protein and erythrocyte sedimentation rate. These results strongly suggest that elevation of CSF IL-6 activity may underly the common pathogenetic mechanism of CNS involvement of vasculitides irrespective of their category. Taken together with the histopathological findings in one patient, the data also suggest that inflammation might not be restricted within the CNS blood vessels, but rather be extended to brain parenchyma to promote IL-6 production presumably by glial cells.
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PMID:Elevation of cerebrospinal fluid interleukin-6 activity in patients with vasculitides and central nervous system involvement. 843 47

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

Extrinsic allergic alveolitis and pulmonary sarcoidosis are granulomatous diseases of the lung for which clinical presentation and anatomic site of granuloma formation differ. Extrinsic allergic alveolitis is caused by inhaled antigens, whereas the nature and source of the inciting antigen in sarcoidosis is unknown. To test the hypothesis that the route via which antigen is introduced to the lung contributes to the clinicopathological presentation of pulmonary granulomatous disease, rats immunized with intravenous (i.v.) Corynebacterium parvum were challenged after 2 weeks with either intratracheal (i.t.) or i.v. C. parvum. The granulomatous inflammation elicited by i.t. challenge predominantly involved alveolar spaces and histologically simulated extrinsic allergic alveolitis. In contrast, the inflammation induced by i.v. challenge was characterized by granulomatous angiitis and interstitial inflammation simulating sarcoidosis. Elevations of leukocyte counts and TNF levels in bronchoalveolar fluid, which reflect inflammation in the intra-alveolar compartment, were much more pronounced after i.t. than after i.v. challenge. Tumor necrosis factor, interleukin-6, CC chemokine, CXC chemokine, and adhesion molecule mRNA and protein expression occurred in each model. In conclusion, i.t. or i.v. challenge with C. parvum in sensitized rats caused pulmonary granulomatous inflammation that was histologically similar to human extrinsic allergic alveolitis and sarcoidosis, respectively. Although the soluble and cellular mediators of granulomatous inflammation were qualitatively similar in both disease models, the differing anatomic source of the same antigenic challenge was responsible for differing clinicopathological presentations.
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PMID:Experimental extrinsic allergic alveolitis and pulmonary angiitis induced by intratracheal or intravenous challenge with Corynebacterium parvum in sensitized rats. 886 77


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