UNIPROT:P05231 - FACTA Search

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Query: UNIPROT:P05231 (interleukin-6)
23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Solutions were formulated to examine, independently, the roles of osmolality and glucose in the reduction of viability and inhibition of phagocyte function by dextrose-containing peritoneal dialysis fluids. The exposure of neutrophils (polymorphonuclear leukocytes) to test fluids containing > or = 2.7% (wt/vol) glucose resulted in significant cytotoxicity as assessed by the release of lactate dehydrogenase above control values (7.12 +/- 2.65%). At the highest concentration of glucose (4.5%), lactate dehydrogenase release was 15.83 +/- 0.49% (P < 0.05). These effects were directly related to the presence of D-glucose in the test fluids. In contrast, phagocytosis and the release of leukotriene B4 from PMN stimulated with serum-treated zymosan were significantly inhibited in an osmolality-, but not glucose-, dependent manner. The inhibition of tumor necrosis factor alpha and interleukin-6 release from mononuclear leukocytes was inhibited by a combination of osmolality and monosaccharide concentration. Under the same conditions, PMN respiratory burst activation remained unaffected irrespective of glucose concentration or fluid osmolality. These data indicate that, in addition to the low pH of peritoneal dialysis fluid and its high lactate concentration, its glucose content (either directly or as a consequence of the resulting hyperosmolality of the fluid) inhibits cell functional parameters. These findings suggest clinically significant inhibition of host defense mechanisms because, in high-glucose dialysis fluids, osmolality does not reach physiologic values, even during extended intraperitoneal dwell periods.
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PMID:Peritoneal dialysis fluid inhibition of phagocyte function: effects of osmolality and glucose concentration. 838 31

The release of free radicals and pro-inflammatory cytokines such as nitric oxide (NO) and tumor necrosis factor alpha (TNF alpha) is commonly observed in adult respiratory distress syndrome (ARDS) following infection or exposure to microbial products. The aim of this study was to scrutinize the involvement of NO in ARDS in a mouse model determined by the sequential exposure to lipopolysaccharide (LPS) and formyl-norleucyl-phenylalanine (FNLP). Nitrite measurements in bronchoalveolar lavage fluids (BALF) and sera demonstrated that exposure to microbial products elicits large amounts of NO in LPS/FNLP-challenged mice. This release was significantly inhibited by infusion with the inducible NO synthase antagonist, aminoguanidine (AG). Our results show that LPS/FNLP exposure induces lung damage as demonstrated by protein and lactate dehydrogenase (LDH) increases in BALF. Liver damage was also detected in LPS/FNLP-challenged mice with increases in serum ornithine-carbamoyltransferase (OCT) levels. LPS/FNLP infusion led to elevated levels of the cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF alpha) in the sera. LPS/FNLP also led to neutrophil adhesion in the lung vasculature, as seen by increased levels of myeloperoxydase. Interestingly, inhibition of NO release in challenged mice led to an important increase in markers of tissue damage in the lungs and livers, but a decrease in neutrophil recruitment. Infusion of AG in LPS/FNLP-challenged mice led to a much increased level of sera TNF alpha. These data suggest that after exposure to microbial products, NO generated as a result of activation of the inducible NO synthase blocks the full expression of tissue damage in the lungs.
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PMID:The involvement of nitric oxide in a mouse model of adult respiratory distress syndrome. 854 74

The legal procedure for evaluating the toxicity of cosmetic, household, chemical and pharmaceutical products is still the irritancy Draize test on rabbits. Various irritation tests are currently being developed as alternatives to in vivo animal testing. Our in vitro model system is composed of 24 equivalent dermis (ED) comprising a chitosan-cross-linked collagen-glycosaminoglycan matrix populated by foreskin fibroblasts. In evaluating this system for irritancy testing, three different measures of toxicity were used: MTT (dimethylthiazol diphenyltetrazolium bromide) reduction, and lactate dehydrogenase and interleukin-6 release. The experiments described herein represent a preliminary evaluation to determine the usefulness and predictive value of our 24 ED kit as an alternative method for the prediction of human dermal reaction, versus three chemical products: cadmium chloride, lauryl sulfate, and benzalkonium chloride. Preliminary results suggest that the ED may be a useful in vitro model for the prediction of cutaneous and ocular toxicity and allow the development of a 24-skin-equivalent kit realized by seeding human normal keratinocytes onto the equivalent dermis.
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PMID:Pharmacotoxicological applications of an equivalent dermis: three measurements of cytotoxicity. 856 46

Inclusion complexes of gamma-cyclodextrin and octamethylcyclotetrasiloxane (D4), decamethyltetrasiloxane (M10TS), and 1,3,5,7-tetramethyltetravinylcyclotetra - siloxane (TMTV-D4) were prepared to compare the cytotoxic effects of siloxanes in vitro. In these preparations, the hydrophobic siloxanes are surrounded by a hydrophilic shell of eight circularly linked D-glucose molecules (gamma-cyclodextrin), and upon contact with plasma membranes the siloxane molecule can intercalate into the lipid bilayer of the cell membrane. XRPC24, 2-11 plasmacytoma, CH12.LX lymphoma and P388D1 macrophage-like cells were used as indicator cells in toxicity assays. Using an MTT tetrazolium reduction to formazan test, a colorimetric method to determine the number of viable cells, the 50% minimal lethal doses (CD50) for the siloxane compounds were found to range from 30 to 50 microM. Sublethal doses (e.g., 15 microM and lower) resulted in the loss of lactate dehydrogenase (LDH) and glutathione (GSH) from the cytosolic compartment of the target cells and thus indicated cytotoxicity. Treatment of macrophages with siloxanes resulted in a higher production of interleukin-6 (IL-6) than was exhibited by untreated macrophages. The B9 cell bioassay of these treated cells showed as much as a 10 fold higher production (500 U/ml) of IL-6 than did the untreated cells. The degree of increase was dependent on the compound and concentration used. The results of this study show that low molecular weight siloxanes produce lethal effects on B-lymphocyte derived target cells in vitro and permeabilize the plasma membranes at lower sublethal concentrations.
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PMID:Cytotoxicity and membrane damage in vitro by inclusion complexes between gamma-cyclodextrin and siloxanes. 856 93

The ability of dicatechol rooperol and esters to inhibit the production of cytokines in endotoxin-stimulated human alveolar macrophages, human blood monocyte/macrophages, histiocytic cell line U937, and rat alveolar macrophages was examined in vitro. Rooperol derivatives inhibited the production of tumour necrosis factor-alpha, interleukin-1 beta and interleukin-6. Of the esters tested on human cells, rooperol diacetate and tetraacetate were more potent inhibitors of cytokine production (IC50 in the range of 10-20 microM) than rooperol disulphate (IC50 in the range of 25-75 microM). The acetate esters also inhibited cytokine production in rat alveolar macrophages, whereas the sulphate had little effect. Rooperol and acetate esters, in the same concentration range, decreased the production of nitric oxide by rat alveolar macrophages stimulated by endotoxin. These concentrations of rooperol had no effect on cell viability, as indicated by incorporation of 14C-labelled leucine into macrophage proteins and their content of lactate dehydrogenase. The results obtained suggest that rooperol esters are potentially useful antiinflammatory agents.
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PMID:Cytokine production in human and rat macrophages and dicatechol rooperol and esters. 883 17

This study examined muscle swelling and changes in inflammatory markers in the blood following eccentric exercise-induced muscle damage. Subjects (N = 14) who had not been involved in a resistance training program performed 24 maximal eccentric actions of the elbow flexors. Muscle swelling was assessed by measures of the upper arm circumference (CIR), ultrasonography (USG), and magnetic resonance imaging (MRI). Plasma concentrations of interleukin-1 alpha, interleukin-1 beta, interleukin-2, interleukin-6, tumor necrosis factor-alpha, and plasma levels of C-reactive protein, cortisol, and zinc were analyzed. Established indicators of muscle damage (maximal isometric force, range of motion, muscle soreness, and plasma creatine kinase, aspartate aminotransferase, and lactate dehydrogenase activities) were also measured. All measures, including CIR and USG, except for MRI, were assessed immediately before and after and for 5 d post-exercise. MRI was taken at pre- and 1, 3, 6, 10, 23, 31, and 58 d post-exercise. All muscle damage indicators changed significantly after exercise. A large increase in CIR (> 20 mm) was found 4-5 d after exercise, and this coincided with USG, showing an increase in muscle thickness. The echointensity of USG increased with the enlargement of the elbow flexors. MRI displayed enlargement of the biceps brachii and brachialis cross-sectional area that started at 1 d, and lasted until 23 d, post-exercise. The most profound increase in the enlargement and signal intensity of the MRI was found 3 or 6 d after exercise. However, none of the plasma levels of inflammatory makers showed significant muscle swelling, which is indicative of muscle edema, but the inflammatory responses after exercise appear to be different from those accompanying infection or tissue injury.
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PMID:Changes in indicators of inflammation after eccentric exercise of the elbow flexors. 887 3

This paper reviews studies in epidemiology, differential diagnosis, clinical manifestations, and treatment of juvenile rheumatoid arthritis (JRA) that have appeared during the past year. One epidemiologic study suggested a decreased incidence recently; however, changes over time in the ethnic and racial characteristics of the patients studied may also have played a role. Findings from an Australian study suggested that some studies may underestimate the true incidence of JRA if visits of physicians are the only basis for the studies. Finally, a Canadian study of incidence showed no seasonal correlations--except for the Prairie region--raising the possibility that the disease varies by region because of environmental factors or variations in ethnic background. Differential diagnostic issues were covered in several reports. One study suggested that elevations in lactate dehydrogenase levels identified children with malignancies who presented with musculoskeletal symptoms. Another study of children with Lyme disease failed to find any patients with asymmetric joint involvement, in contrast to JRA patients. Two studies from Europe reached opposite conclusions regarding whether the incidence of celiac disease was increased in JRA patients. Clinical studies included a French study showing increased production of interleukin-6 and interleukin-1-Ra during fever spikes in children with systemic JRA. An Italian study explored the potential role of interleukin-6 in the anemia of JRA patients. An American study confirmed decreases in markers of bone formation in JRA patients. Two treatment studies addressed the use of intravenous gamma globulin in JRA. Another report described two JRA patients who developed nodules while receiving methotrexate. Finally, a report added confirmation to the successful use of cyclosporine for macrophage activation syndrome in JRA.
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PMID:Clinical aspects of juvenile rheumatoid arthritis. 930 97

Recent studies have emphasized the role of peritoneal mesothelial cell (PMC) in peritoneal immune defense mechanisms in continuous ambulatory peritoneal dialysis (CAPD). The aim of this study was to evaluate a possible relationship between peritoneal dialysis effluent (PDE), cytokine (Cy) levels, and PMC viability and their impact on peritonitis morbidity. Fifteen patients initiating CAPD for end-stage renal failure participated in the study. The following parameters were evaluated: (1) the levels of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-6 (IL-6), and interleukin-8 (IL-8) in PDE samples taken 7 days after initiating CAPD, at the end of the first, third, and sixth month of CAPD (determined by a solid phase enzyme amplified sensitivity immunoassay EASIA); (2) peritoneal mesothelial cell viability [determined by the release of lactate dehydrogenase (LDH) and by trypan blue extrusion test] by isolating and culturing peritoneal mesothelial cells at the moment of the placement of the peritoneal catheter and at the sixth month of CAPD; (3) peritonitis incidence during the 24 months after starting CAPD. At the first month of CAPD in all patients there was a slight increase in PDE IL-1 beta and TNF-alpha levels, while other Cy were almost undetectable. Time course studies showed that in 10 patients (Group I) there was a significant increase in PDE levels of IL-6, IL-8, and INF-gamma (p < 0.0005) in comparison to other Cy and a good PMC viability. In the other 5 patients (Group II) there were higher PDE levels of IL-1 beta and TNF-alpha (p < 0.0005). This was associated with a marked reduction in PMC viability determined by the release of LDH and by the trypan blue extrusion test. During the 24 months after starting CAPD, incidence of peritonitis was one episode per 24 patient-months in Group I and one episode per 9.2 patient-months in Group II. Our results show that from the beginning of CAPD there are distinct patterns of Cy in the PDE that correlate with a different PMC viability and peritonitis morbidity. Thus the analysis of the above-mentioned parameters may be useful in the early identification of the risk of peritonitis, thus allowing preventive measures.
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PMID:Peritoneal dialysis effluent, cytokine levels, and peritoneal mesothelial cell viability in CAPD: a possible relationship. 936 Jun 42

It is well known that ozone (O3) causes acute lung inflammation. What is not known is whether there is progression of the inflammatory response in humans with repeated short-term exposures. Our study was designed to test the hypothesis that repeated exposures to a high-ambient concentration of O3 (0.2 ppm) over several days would cause more inflammation than a single exposure. Fifteen healthy volunteers were exposed in random fashion to 0.2 ppm ozone for 4 h on a single day and to 0.2 ppm O3 for 4 h on 4 consecutive days while exercising moderately for 30 min of each hour. Pulmonary function tests were obtained immediately before and after each 4-h exposure. Bronchoscopy was performed 20 h after the completion of each exposure arm to obtain bronchoalveolar lavage (BAL) for measurement of markers of inflammation. Our results show initial progression followed by attenuation of the acute physiologic response to O3 with repeated daily exposures. We found a significant difference in percent change in FEV1, FVC, and specific airway resistance (SRaw) across the single-day exposure when compared with the change across Day 4 of the 4-d exposure. Bronchial fraction (the first 15 ml of BAL return) and BAL were analyzed for the following end points: total and differential cell counts, total protein, lactate dehydrogenase (LDH), fibronectin, interleukin-6 (IL-6), interleukin-8 (IL-8), and granulocyte-macrophage colony-stimulating factor (GM-CSF). In the bronchial fraction the number of polymorphonuclear cells (PMN)s and fibronectin concentration were significantly decreased after 4-d exposure compared with single-day exposure. In BAL, significant decreases in the number of PMNs, fibronectin, and IL-6 were found after 4-d exposure versus single-day exposure. These results suggest that there is attenuation of the O3-induced inflammatory response in both proximal airways and distal lung with repeated daily exposures.
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PMID:Ozone-induced inflammation is attenuated with multiday exposure. 970 Jan 32

A 71-year-old woman with multiple myeloma (MM) in remission was admitted for evaluation of recent abdominal distension and was diagnosed as having massive myeloma ascites. The fluid was characterized by a total nucleated cell count of 6,600/mm3 (67% plasma cells), with a plasma cell CD38+ phenotype. Chemical analysis of the fluid showed lactate dehydrogenase of 122 IU/L, total protein of 2.9 g/dL, albumin of 2.4 g/dL, diastase of 38 IU/dL, cholesterol of 46 mg/dL, and C-reactive protein of 3 g/dL. The serum-ascites albumin gradient (SAAG) was low (0.9). Electrophoresis of the ascitic fluid showed a monoclonal spike in the gamma region and immunoelectrophoresis confirmed the presence of lambda light chains similar to those seen in the urine. Further analysis of the ascitic fluid showed markedly elevated levels of beta2 microglobulin (11,161 microg/L) and interleukin-6 (146 pg/ml compared to serum level of 4.3 pg/ml). There was evidence of intraabdominal masses that completely resolved with continuous high-dose cyclophosphamide (750 mg/m2/day for four days) followed by clinical improvement and disappearance of the ascites. We stress the value of complete fluid characterization and intensive chemotherapy to achieve a favorable outcome.
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PMID:Myeloma ascites--a favorable outcome with cyclophosphamide therapy. 992 7

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