acetylcellulose has been researched along with Inflammation* in 7 studies
1 review(s) available for acetylcellulose and Inflammation
1 trial(s) available for acetylcellulose and Inflammation
6 other study(ies) available for acetylcellulose and Inflammation
| Article | Year |
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Physiological heating augments the anti-inflammatory reactions during granulocyte/monocyte apheresis: A in vitro study.
Granulocyte and monocyte adsorptive apheresis (GMA), an effective therapy for inflammatory disorders, exerts an anti-inflammatory influence by utilizing the biological reaction between blood and cellulose acetate (CA) beads, which are the carriers of the GMA column. Although the biological reaction has an optimum temperature, blood contacts the CA beads below body temperature as GMA is performed in an extracorporeal circulation system. We investigated various soluble factors in blood treated with CA beads at 25°C and 37°C. Here, the optimal temperature for IL-1 receptor antagonist (IL-1ra) release induced by CA beads was 37°C, and IL-6 production from monocytic cells was inhibited by the addition of plasma prepared from the CA bead-treated blood at 37°C, rather than at 25°C. These results indicated that physiological heating of the apheresis carrier augmented the anti-inflammatory reaction in vitro. Thus, heating during GMA may be a new approach for augmenting clinical efficacy. Topics: Anti-Inflammatory Agents; Blood Component Removal; Cellulose; Granulocytes; Hot Temperature; Humans; In Vitro Techniques; Inflammation; Monocytes | 2021 |
Vitamin E-coated cellulose acetate dialysis membrane: long-term effect on inflammation and oxidative stress.
Chronic inflammation and oxidative stress are prevalent in hemodialysis (HD) patients. We evaluated the long-term effect of a vitamin E-coated cellulose acetate (CAE) membrane on oxidative stress and inflammation.. Nine patients were switched to CAE membrane for 3 months and then changed back to polysulfone (PS) membrane again for 6 months. Reactive oxygen metabolites and derivatives (d-ROMs), total antioxidant capacity (TAC) and superoxide dismutase (SOD) (oxidative stress biomarkers), high-sensitivity C-reactive protein (Hs-CRP), and interleukin-6 (IL-6) (inflammation biomarkers) were measured.. d-ROMs decreased and TAC rose significantly at the end of the study, whereas SOD increased rapidly and immediately after the end of CAE treatment. Hs-CRP and IL-6 levels were significantly lowered at the end of the study.. Vitamin E supplementation by vitamin E-coated CAE dialysis membrane suppresses oxidative stress and inflammation. Topics: Aged; Antioxidants; C-Reactive Protein; Cellulose; Coated Materials, Biocompatible; Female; Free Radicals; Humans; Inflammation; Interleukin-6; Kidney Failure, Chronic; Male; Membranes, Artificial; Middle Aged; Oxidative Stress; Polymers; Reactive Oxygen Species; Renal Dialysis; Sulfones; Superoxide Dismutase; Vitamin E | 2010 |
Coagulation cascade activation causes CC chemokine receptor-2 gene expression and mononuclear cell activation in hemodialysis patients.
Priming of the coagulation cascade during hemodialysis (HD) leads to the release of activated factor X (FXa). The binding of FXa to its specific receptors, effector protease receptor-1 (EPR-1) and protease-activated receptor-2 (PAR-2), may induce the activation of peripheral blood mononuclear cells (PBMC) and promote a chronic inflammatory state that is responsible for several HD-related morbidities. In the attempt to elucidate the mechanisms underlying the coagulation-associated inflammation in HD, 10 HD patients were randomized to be treated subsequently with a cellulose acetate membrane (CA) and Ethylen-vinyl-alcohol (EVAL), a synthetic membrane that has been shown to reduce FXa generation. At the end of each experimental period, surface FXa and thrombin receptors (EPR-1 and PAR-1, -2, and -4) and CCR2 (monocyte chemoattractant protein-1 receptor) gene expression in isolated PBMC were examined. the ability of dialytic membranes to activate protein-tyrosine kinases and the stress-activated kinase JNK and to modulate the generation of terminal complement complex (TCC) was also investigated. EPR-1 and PAR-2 and -4 mRNA expression, barely detectable in normal PBMC, were significantly upregulated in HD patients, particularly in those who were treated with CA. A striking increase of tyrosine-phosphorylated proteins and JNK activation was observed at the end of HD only in CA-treated patients. Simultaneously, an increased gene expression for both splicing isoforms of CCR2, A and B, only in PBMC from CA-treated patients was demonstrated. The increased CCR-2 mRNA abundance was followed by a significant increase in its protein synthesis. The high expression of CCR2 was associated with an increased generation of plasma TCC and a significant drop in leukocyte and monocyte count. By contrast, EVAL treatment slightly lowered TCC generation and normalized leukocyte count. In vitro FXa induced CCR2 A and B expression and JNK activation in freshly isolated PBMC. FXa-induced CCR2 mRNA expression was completely abolished by JNK and tyrosine kinase inhibition. In conclusion, these data suggest that subclinical clotting activation may cause an increased CCR2 gene and protein expression on uremic PBMC, contributing to HD-related chronic microinflammation. The use of the less coagulation-activating membrane, EVAL, may reduce PBMC activation through the modulation of the stress-activated kinase JNK. Topics: Adult; Aged; Apoptosis Regulatory Proteins; Blotting, Western; Cell Membrane; Cellulose; Complement Membrane Attack Complex; DNA-Binding Proteins; Enzyme Inhibitors; Factor Xa; Female; Gene Expression Regulation; Humans; Inflammation; Leukocytes; Leukocytes, Mononuclear; Male; MAP Kinase Kinase 4; Middle Aged; Monocytes; Phosphorylation; Polyvinyls; Protein Binding; Protein Isoforms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-ets; Receptor, PAR-1; Receptor, PAR-2; Receptors, CCR2; Receptors, Chemokine; Renal Dialysis; Reverse Transcriptase Polymerase Chain Reaction; RNA; RNA, Messenger; Time Factors; Transcription Factors | 2005 |
Effect of changing from a cellulose acetate to a polysulphone dialysis membrane on protein oxidation and inflammation markers.
In vitro, synthetic dialysis membranes induce less activation of blood components to produce pro-inflammatory cytokines and reactive oxygen species compared with cellulose acetate membranes. However, the long-term effect of switching from a cellulose-based dialysis membrane to a synthetic membrane on protein oxidation and systemic inflammation in hemodialysis patients is not well defined.. Nineteen patients receiving hemodialysis were followed prospectively after changing from a low-flux cellulose acetate membrane to a low-flux polysulphone membrane for 11-17 months (n = 15) and then returning to the cellulose acetate membrane for 1 month (n = 13). Plasma markers of protein oxidation, cell activation and systemic inflammation and concentrations of soluble cell adhesion molecules were measured at baseline and at the end of each intervention period.. Plasma levels of protein thiols (18%), IL-6 (34%), VCAM-1 (33%), ICAM-1 (21%) and beta2-microglobulin (21%) increased significantly and dityrosine fluorescence (-36%), protein lipofuscin-like fluorophores (-18%) and TNF-alpha (-20%) decreased significantly in the patients after they switched to the polysulphone membrane. After reverting to the cellulose acetate membrane for 1 month, plasma levels of protein thiols and IL-6 returned to baseline while levels of other variables were not significantly different from values at the end of the polysulphone dialysis period. There was substantial intra-individual variation between 2 baseline measurements of plasma cytokines.. Switching from a cellulose acetate membrane to a low-flux polysulphone dialysis membrane for a year or more may decrease the level of protein oxidation suggesting a decrease in oxidant stress and greater biocompatibility of the polysulphone membrane. The effect of this change in dialysis membrane on systemic inflammation is uncertain due to increases in some but not other inflammation-sensitive molecules. Topics: Blood Proteins; Cellulose; Cytokines; Female; Hemodialysis, Home; Humans; Inflammation; Kidneys, Artificial; Male; Membranes, Artificial; Middle Aged; Oxidation-Reduction; Polymers; Prospective Studies; Sulfones | 2004 |
Effect of cellulose acetate materials on the oxidative burst of human neutrophils.
Following adverse clinical events involving seven patients undergoing renal dialysis using 12-year-old cellulose acetate hemodialyzers, this in vitro study was proposed in an effort to characterize the inflammatory response to the constituent cellulose acetate (CA) fiber materials. Chemiluminescence (CL) and apoptosis assays were used to determine whether human neutrophils were activated by CA fiber materials and/or are sensitive to degradation/alteration of these fibers over time. Furthermore, the study examined in vitro assays with human neutrophils using a CA film, the solvents used in the film preparation and CA resin. The film could be cut to identical sized pieces in an effort to compare hemodialysis material effects in standardized amounts. For the CL assays, 60-min exposure was followed by secondary stimulation with n-formyl-met-leu-phe (fMLP) or phorbol-12-myristate-13-acetate (PMA). Short-term exposure (60-min postintroduction to CA materials) increased the inflammatory response as measured by the respiratory burst of neutrophils (p < or =.05), with CA fiber exposure significantly compared with cells alone. There was a trend toward an increased response with exposure to older fibers with secondary PMA stimulation. Apoptosis was increased 12% with exposure to the more aged fibers versus 2% with the new fibers. The fiber storage component, glycerol, significantly inhibited the oxidative response (p < or =.001; > or =80% suppression with concentrations of 5-20%). The solvents used in film preparation, N,N-dimethylacetamide and tetrahydrofuran, produced greater than a 70% and 60% suppression, respectively, of CL activity for all concentrations > or =1%. More work is needed to determine the specific nature of the interaction of inflammatory cells with CA materials, but early evidence suggests that neutrophils are activated by CA and display an altered response to more aged fibers. Topics: Adult; Apoptosis; Biocompatible Materials; Cellulose; Humans; In Vitro Techniques; Infections; Inflammation; Kidneys, Artificial; Luminescent Measurements; Materials Testing; Neutrophils; Renal Dialysis; Respiratory Burst; Time Factors | 2001 |
Acute-phase proteins during hemodialysis: correlations with serum interleukin-1 beta levels and different dialysis membranes.
The effects of hemodialysis (HD) on the levels of serum amyloid A (SAA), C-reactive protein (CRP) and interleukin-1 beta (IL-1 beta) were studied in 8 patients. Bicarbonate dialysate was used exclusively, and three different membranes, Cuprophan (CU), cellulose acetate (CA), and polymethylmetachrylate (PMMA) were compared. The SAA levels increased significantly with each membrane. With CU, they rose from 4.0 +/- 2.0 (mg/l, mean +/- SEM) to 9.6 +/- 2.8 at 60 min and to 15.0 +/- 4.9 at 240 min. The values with CA were 3.8 +/- 2.1, 15.3 +/- 5.6, and 23.8 +/- 3.9; and with PMMA 2.4 +/- 1.3, 12.1 +/- 5.6, and 12.1 +/- 5.9, respectively. The alterations of SAA neither correlated with the weight loss nor the increase of serum albumin during dialysis. The CRP values showed insignificant changes. The IL-1 beta levels rose with CU from 87 +/-18 (ng/l) to 155 +/- 33 at 60 min and to 172 +/- 47 at 240 min. With CA, the values were 67 +/- 14, 198 +/- 46, and 121 +/- 23, and with PMMA 63 +/- 13, 246 +/- 93, and 211 +/- 86, respectively. These results did not correlate with the effects of the membranes on complement activation. It is concluded that the release of cytokines during HD apparently leads to a rapid synthesis of acute-phase proteins as a sign of inflammation. Thus, SAA may be used as one indicator of the biocompatibility of HD treatment. Topics: Adult; Aged; C-Reactive Protein; Cellulose; Complement Activation; Cytokines; Female; Humans; Inflammation; Interleukin-1; Leukopenia; Male; Membranes, Artificial; Methylmethacrylates; Middle Aged; Renal Dialysis; Serum Amyloid A Protein | 1991 |