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)

As an immunomodulator, melatonin reportedly exhibits protective effects in severe sepsis/shock induced by bacterial lipopolysaccharides in animal models. The present study was conducted to evaluate the possible protective effects of melatonin against experimental Candida sepsis in rats. A total of 40 adult male Wistar rats were randomly assigned to 4 groups: control, melatonin-treated control, septic, and melatonin-treated septic. Melatonin (200 microg/kg/d, intraperitoneally) injections were begun a week prior to sepsis induction and were continued daily for 3 wk until the end of the study. Cyclophosphamide was administered to animals in all groups as an immunosuppressive agent as a single dose 4 d prior to yeast inoculation. To cause sepsis, the Candida albicans (ATCC 10259) strain was administered intravenously. Amphotericin B was given as an antimycotic therapeutic agent as a single dose to septic rats. Plasma levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), vascular cell adhesion molecule-1, and E-selectin were measured on the first and 15th days of sepsis. IL-6, TNF-alpha, vascular cell adhesion molecule-1, and E-selectin levels of septic rats were higher than those of controls. Melatonin reduced IL-6 levels and shortened time to improvement in animals with Candida sepsis. Levels of TNF-alpha and adhesion molecules in melatonin-treated septic rats were decreased compared with those in septic rats, but this difference was not statistically significant. In light of the current results, investigators conclude that melatonin may have therapeutic benefits in Candida sepsis and in classic antimycotic treatment because of its immune regulatory effects.
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PMID:Effects of melatonin on Candida sepsis in an experimental rat model. 1752 65

Inflammatory markers, their relation to maintenance of sinus rhythm after electrical cardioversion for atrial fibrillation (AF), and the effect of candesartan were investigated in a double-blind placebo-controlled study (CAPRAF). One hundred seventy-one patients with persistent AF were randomly assigned to receive candesartan 8 mg/day or placebo for 3 to 6 weeks before and candesartan 16 mg/day or placebo for 6 months after electrical cardioversion. Serum levels of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha, interleukin-6, P-selectin, E-selectin, CD-40 ligand, and vascular cell adhesion molecule-1 were measured at baseline and end of study. Compared with patients with a relapse of AF, patients still in sinus rhythm at 6 months after cardioversion (n = 40) had lower baseline hs-CRP and E-selectin levels: median 2.36 mg/L (25th, 75th percentiles 1.28, 4.09) versus 3.44 mg/L (25th, 75th percentiles 1.66, 6.05, p = 0.031) and 32 ng/ml (25th, 75th percentiles 23, 42) versus 37 ng/ml (25th, 75th percentiles 28, 51, p = 0.042), respectively. Neither sustained sinus rhythm for 6 months nor treatment with candesartan had an impact on measured concentrations of markers of inflammation. In conclusion, low hs-CRP and E-selectin at baseline were associated with maintenance of sinus rhythm after electrical cardioversion.
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PMID:Effect of candesartan and various inflammatory markers on maintenance of sinus rhythm after electrical cardioversion for atrial fibrillation. 1753 93

Skin wound healing is mediated by inflammatory cell infiltration that is highly regulated by various adhesion molecules. Mice lacking intercellular adhesion molecule-1 (ICAM-1) delayed skin wound healing and mice lacking both L-selectin and ICAM-1 (L-selectin/ICAM-1(-/-)) show more delayed wound healing. Deficiency of both endothelial selectins (E-selectin or P-selectin) also delays wound healing. However, the relative contribution and interaction of selectins and ICAM-1 to the wound healing remain unknown. To clarify them, repair of excisional wounds was examined in L-selectin/ICAM-1(-/-) mice, wild-type mice with both E- and P-selectin blockade, and L-selectin/ICAM-1(-/-) mice with both E- and P-selectin blockade. Wild-type mice with both E- and P-selectin blockade showed delayed wound healing that was comparable with that in L-selectin/ICAM-1(-/-) mice. Combined E- and P-selectin blockade in L-selectin/ICAM-1(-/-) mice resulted in more significant delay. Mice lacking or blocked for adhesion molecules also showed suppressed keratinocyte migration, angiogenesis, granulation tissue formation, leukocyte infiltration, and cytokine expression, including transforming growth factor-beta and interleukin-6. Application of basic fibroblast growth factor (bFGF) but not platelet-derived growth factor to the wounds significantly improved wound healing in L-selectin/ICAM-1(-/-) mice with both E- and P-selectin blockade. bFGF significantly increased the leukocyte infiltration and subsequent fibrogenic cytokine production, as well as keratinocyte migration, angiogenesis, and collagen synthesis despite the loss of four kinds of adhesion molecules. These results indicate that skin wound healing is regulated cooperatively by all selectins and ICAM-1 and may provide critical information for the therapy of skin wounds.
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PMID:Endothelial selectins regulate skin wound healing in cooperation with L-selectin and ICAM-1. 1759 78

Sixty cases with primary knee OA were equally categorized into six groups with EHI (Gs 1, 2, 3) or without (Gs 4, 5, 6). GI included cases with HCV, GII cases with RHS & HCV and GIII cases with a history of non-active schistosomiasis whereas Gs 4, 5 & 6 included cases without EHI. Clinical examination with inclusion criteria of pathological manifestations w\as associated with biochemical evaluation of adhesion molecules (E-selectin, P-selectin, intracellular adhesion molecule-3 "ICAM-3") in plasma and synovial fluid. Synovial fluid indices (IgG, IgA, IgM, & C3) were evaluated as well as indices of inflammation and oxidative stress (Beta 2 microglobulin, Haptaglobulin, fibronectin, total thiol, superoxide dismutase, thiobarbituric acid reactive substance & hyaluronan) in synovial fluid and indices activating fibrogenesis in serum and plasma (procollagen III, plasma prolidase, Interleukin-1 beta, Interleukin-6 & TNF alpha). The results showed a positive relationship between indices activating vascular damage, fibrogenesis and immuno-inflammatory response with higher change magnitude in EHI cases particularly with combined HCV & RHS. This implement the dual role of hepatic insult and intestinal amoebiasis on immune mediated mechanisms activating inflammatory response in OA cases reflecting common signaling pathways associated with pathogenesis of multifaceted origin.
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PMID:Dual impact of chronic liver disease and amaebiasis on immunopathogenesis of primary osteoarthritis in Egyptians. 1792 12

Increased deposition of amyloid beta (Abeta) is characteristic for normal aging and human immunodeficiency virus-1 (HIV-1)-associated alterations of the central nervous system. In addition, both Abeta and HIV-1 are known to induce cellular oxidative stress and disruption of the blood-brain barrier (BBB). Therefore, we hypothesize that Abeta and HIV-1 protein Tat can potentiate their proinflammatory effects at the brain endothelium level. To address this hypothesis, we studied promoter activity of three proinflammatory genes in an in vitro BBB model of human brain microvascular endothelial cells (HBMEC) cocultured with a human astrocyte cell line producing Tat (SVGA-Tat cells) and exposed to Abeta. Treatment of HBMEC with Abeta(1-40) in the presence of SVGA-Tat cells resulted in a significant up-regulation of E-selectin, CC chemokine ligand-2, and interleukin-6 promoter activities and protein levels compared with the individual effects of Abeta or Tat. In addition, Abeta markedly amplified E-selectin promoter activity in HBMEC cocultured with HIV-1-infected Jurkat T cells. Simvastatin, the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, effectively blocked proinflammatory reactions induced by Abeta in cocultures with SVGA-Tat cells or with HIV-1-infected Jurkat cells. The present study indicates that a combined exposure to Abeta and Tat or HIV-1 can synergistically potentiate the expression of inflammatory genes in brain endothelial cells. In addition, simvastatin may provide a beneficial influence by reducing these effects at the BBB level.
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PMID:Simvastatin protects against amyloid beta and HIV-1 Tat-induced promoter activities of inflammatory genes in brain endothelial cells. 1827 75

To characterize early blood and tissue markers predictive of decompression sickness (DCS), this study focused on identifying changes in inflammatory mediators during the 24-h period immediately following compression-decompression of female Sprague-Dawley rats. Early blood and tissue markers predictive of DCS include inflammatory cytokines and cell adhesion molecules (CAMs). Increased levels of inflammatory cytokines, especially tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interferon-gamma (IFN-gamma), were detected in the circulation 6 h after decompression. Increased levels of only IL-6 were observed at 24 h. Compared with control animals maintained at 1 atmospheres absolute pressure ATA (101 kPascal), significant increases in expression of E-selectin, and L-selectin, as well as intercellular adhesion molecule-1 (ICAM-1), were observed immunohistochemically in the lungs and brains of the rats 6 h after exposure to 2 (203 kPascal), 3 (303 kPascal), or 4 (404 kPascal) ATA, followed by rapid decompression. These levels drop by 24 h. In contrast to the observations in brain, greater increases in expression of E-selectin and L-selectin around vessels and connective tissue were seen at 24 h after decompression in the quadriceps of rats exposed to either 3 or 4 ATA. Significant increases in expression of the A(2A) receptor, which modulates inflammation by downregulating production of these cytokines, were detected only in the quadriceps removed at 24 h after decompression from 4 ATA. This study demonstrated that rapid decompression induces the release of mediators of inflammation and resulting tissue inflammation cascades, as well as a protective anti-inflammatory response.
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PMID:Inflammatory cytokines and cell adhesion molecules in a rat model of decompression sickness. 1827 1

Enterohemorrhagic Escherichia coli (EHEC) induces hemorrhagic colitis and hemolytic uremic syndrome (HUS). Morbidity and mortality are increased in HUS patients with neurologic complications. To determine the pathogenesis of the central nervous system (CNS) involvement in HUS by EHEC, we determined the serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptor 1 (sTNFR1), IL-10, interferon-gamma (IFN-gamma), IL-2, IL-4, soluble E-selectin (sE-selectin), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) during the acute stage in children with HUS with or without CNS involvement. Serum concentrations of IL-6, IL-10, sTNFR1, sE-selectin, MMP-9, and TIMP-1, but not TNF-alpha, IFN-gamma, IL-2, or IL-4, were significantly higher in patients with HUS with encephalopathy compared with controls. Serum IL-6, sTNFR1 and TIMP-1 concentrations were significantly higher in patients with HUS with encephalopathy compared with those with HUS without encephalopathy (P=0.031, P=0.005, and P=0.007, respectively) and those with acute colitis without HUS (P=0.011, P<0.001, and P=0.005, respectively). There were no significant differences in hemoglobin, platelet counts, leukocyte counts, or serum concentrations of IL-10, sE-selectin, MMP-9, aspartate aminotransferase, lactate dehydrogenase, blood urea nitrogen, creatinine, or C-reactive protein between the HUS patients with and without encephalopathy. Our preliminary study suggests that serum IL-6, sTNFR1 and TIMP-1 levels, particularly sTNFR1 and TIMP-1, are important for predicting neurological complications in patients with HUS.
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PMID:Soluble tumor necrosis factor receptor 1 and tissue inhibitor of metalloproteinase-1 in hemolytic uremic syndrome with encephalopathy. 1841 Sep 71

The aims of the study are (1) assessment of cell surface expression of adhesion molecules CD11b and CD62L on peripheral blood neutrophils in patients with type 2 diabetes and microangiopathy; (2) analysis of serum levels of soluble adhesion molecules: E-selectin (sE-selectin), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and von Willebrand factor (vWF) and; (3) evaluation of systemic inflammatory markers like interleukin-6 (IL-6), soluble interleukin-6 receptor (IL-6Rs), high sensitivity C-reactive protein (hsCRP) and fibrinogen. Thirty patients with type 2 diabetes and microangiopathy were enrolled in the study. The study group was compared to 22 patients with type 2 diabetes without microangiopathic compliations. The control group included 20 healthy volunteers. Flow cytometry was used to analyse surface expression of adhesion molecules. Both inflammatory markers and soluble adhesion molecules were determined by immunoenzymatic assay. A significant increase in neutrophil surface CD11b expression (P < 0.01) as well as decrease in surface CD62L expression (P < 0.01) were observed in the group with diabetic microangiopathy in comparison with diabetic group without microangiopathic complications and healthy controls. Moreover, significantly higher concentrations of sICAM-1 (P < 0.05), sVCAM-1 (P < 0.05), sE-selectin (P < 0.05), vWF (P < 0.01), hsCRP (P < 0.01), IL-6 (P < 0.01) and fibrinogen (P < 0.001) were also found in patients with microangiopathy in comparison with the control group. IL-6Rs concentrations did not significantly vary between groups. We concluded (1) diabetic microangiopathy is accompanied by increase in CD11b expression and decrease in CD62L expression on peripheral blood neutrophils; (2) in diabetic microangiopathy rise in CD11b expression indicates neutrophil activation and intensified adhesion; (3) the development of diabetic microangiopathy is accompanied by an increase in soluble adhesion molecules and inflammatory markers concentrations in the blood.
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PMID:Neutrophil surface expression of CD11b and CD62L in diabetic microangiopathy. 1849 41

Rheological properties of erythrocytes from patients with high risk of cardiovascular disease (CVD) were analyzed in relation to individual patient risk factors as well as to the medication. Additionally, comparative statistical analysis was performed considering plasma concentration of the selected mediators of vascular endothelium: 6-keto-prostaglandin F(1alpha) (PGF(1alpha)), sVCAM-1 and E-selectin adhesion molecules and interleukin-6 (IL-6). It was found that antihypertensive therapy with angiotensin-converting enzyme inhibitor (ACEI) is accompanied by improvement of RBC rheology: the increase of deformability and the decrease of aggregability. This improvement is probably mediated by endothelial prostacyclin and nitric oxide which are generated by ACEI. A correlation was observed between RBC deformability/aggregability and the patient's hematocrit level, what implicates that the hematocrit level should be explicitly taken into consideration when investigating rheological properties of erythrocytes. A strong relationship was also found between the plasma concentration of sVCAM-1 and patient's age.
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PMID:Rheological properties of erythrocytes in patients with high risk of cardiovascular disease. 1850 28

The immunogenic properties of renal cell carcinoma (RCC) on bone osteolysis were investigated. mRNA expression of three proinflammatory cytokines, monocyte chemotactic protein-1 (MCP-1), interleukin-6 (IL-6) and interleukin-8 (IL-8), were determined in a panel of RCC lines (CRBM 1990, ACHN and Caki-1). Moreover proinflammatory cytokine mRNA expression and protein levels of adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and E-selectin, on human umbilical vein endothelial cells (HUVEC) incubated with the conditioned media from RCC lines were evaluated. RCC express mRNA of MCP-1, IL-6 and IL-8 that may induce a proinflammatory phenotype in endothelial cells. mRNA expression of IL-6, and IL-8 was induced on HUVEC treated with the conditioned media from RCC lines and mRNA and protein levels of ICAM-1 and E-selectin were also increased. This study demonstrates the immunogenic properties of renal cell carcinoma, such as pro-inflammatory cytokine secretion and the induction of adhesion molecules (ICAM-1 and E-Sel) by endothelial cells. ICAM-1 binds lymphocyte function-associated antigen-1 (LFA-1), which is expressed by pre-osteoclasts, so that, the observed proinflammatory phenotype in HUVEC may also favour osteoclast recruitment in bone metastases microenvironment. Osteolysis in bone metastases, mediated by this pathway, may be further potentiated by the pro-angiogenic properties of RCC.
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PMID:Immunogenic properties of renal cell carcinoma and the pathogenesis of osteolytic bone metastases. 1936 Mar 51


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