The flavonoids comprise a large class of low-molecular-weight plant metabolites ubiquitously distributed in food plants. These dietary antioxidants exert significant antitumor, antiallergic, and anti-inflammatory effects. The molecular mechanisms of their biological effects remain to be clearly understood. We investigated the anti-inflammatory potentials of a safe, common dietary flavonoid component, quercetin, for its ability to modulate the production and gene expression of the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) by human peripheral blood mononuclear cells (PBMC). Our results showed that quercetin significantly inhibited TNF-α production and gene expression in a dose-dependent manner. Our results provide direct evidence of the anti-inflammatory effects of quercetin by PBMC, which are mediated by the inhibition of the proinflammatory cytokine TNF-α via modulation of NF-κβ1 and Iκβ. ...
Intravenous injection of Candida albicans into mice produced elevated serum tumor necrosis factor alpha (TNF-alpha) levels. We hypothesized that immunostimulants released in vivo from C. albicans during fungal sepsis might contribute to the elevated levels of TNF-alpha in serum. We tested this hypothesis in mice with C. albicans mannan (CAM). Increased serum TNF-alpha levels were observed following intravenous and intraperitoneal injections of CAM. Injection of CAM into mice resulted in increased serum TNF-alpha concentrations that reached 1,200 pg/ml of blood, compared with 2,400 microg/ml of blood following injection of 10 microg of endotoxin. The response to CAM was concentration dependent, requiring a minimum dose of 20 microg of CAM per g of body weight. Sera from mice were tested 30, 60, 90, and 120 min after intravenous injections with CAM. TNF-alpha concentrations were minimal 30 and 120 min after intravenous injection and maximal 60 and 90 min after CAM injection. The relative ...
Endogenous tumor necrosis factor alpha is required for enhanced antimicrobial activity against Toxoplasma gondii and Listeria monocytogenes in recombinant gamma
TY - JOUR. T1 - Antiviral effects of recombinant human tumor necrosis factor-alpha in combination with natural interferon-beta in mice infected with herpes simplex virus type 1. AU - Schmitt, David A.. AU - Sasaki, Hidetaka. AU - Pollard, Richard B.. AU - Suzuki, Fujio. PY - 1992/10/1. Y1 - 1992/10/1. N2 - The protective effects of combination therapy utilizing recombinant human TNF-alpha (rTNF-α) and natural murine interferon-beta (IFN-β) in mice infected with herpes simplex virus type 1 (HSV-1) was investigated. Mice treated with rTNF-α alone at all of the doses tested (a single i.v. administration, 2.3-2,300 μg/kg; multiple i.p. administrations 0.4-250 μg/kg) as well as mice that received IFN-β alone at doses of 16 × 104 U/kg or less resulted in a 0% survival rate. Combination therapy consisting of a single administration of rTNF- α (230 and 23 μg/kg) and multiple administrations of IFN-β (4 × 104 U/kg) resulted in a 40% and 60% survival rate. Multiple treatments of infected mice ...
TY - JOUR. T1 - Modulation of lipopolysaccharide-induced tumor necrosis factor-α and nitric oxide production by dopamine receptor agonists and antagonists in mice. AU - Haskó, G.. AU - Szabó, C.. AU - Merkel, K.. AU - Bencsics, A.. AU - Zingarelli, B.. AU - Kvetan, V.. AU - Vízi, E.. PY - 1996/3. Y1 - 1996/3. N2 - The effects of various agonists and antagonists of dopamine D1 and D2 receptors on lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) and nitric oxide (NO) production was investigated in mice. Pretreatment of animals with bromocryptine or quinpirole, agonists of dopamine D2 receptors caused a blunting of both the TNF-α and MO responses to LPS injected intraperitoneally. Sulpiride, an antagonist of dopamine D2 receptors, decreased the LPS-induced TNF-α plasma levels in a dose-dependent manner and inhibited the LPS-induced NO production by peritoneal macrophages. Bromocryptine or quinpirole blunted both the TNF-α and NO response to LPS. SCH-23390, an antagonist of ...
The human tumor necrosis factor alpha (TNF-alpha) gene is one of the earliest genes transcribed after the stimulation of a B cell through its antigen receptor or via the CD-40 pathway. In both cases, induction of TNF-alpha gene transcription can be blocked by the immunosuppressants cyclosporin A and FK506, which suggested a role for the NFAT family of proteins in the regulation of the gene in B cells. Furthermore, in T cells, two molecules of NFATp bind to the TNF-alpha promoter element kappa 3 in association with ATF-2 and Jun proteins bound to an immediately adjacent cyclic AMP response element (CRE) site. Here, using the murine B-cell lymphoma cell line A20, we show that the TNF-alpha gene is regulated in a cell-type-specific manner. In A20 B cells, the TNF-alpha gene is not regulated by NFATp bound to the kappa 3 element. Instead, ATF-2 and Jun proteins bind to the composite kappa 3/CRE site and NFATp binds to a newly identified second NFAT site centered at -76 nucleotides relative to the ...
TY - JOUR. T1 - Nutritional parameters observed during 28-day infusion of recombinant human tumor necrosis factor-α. AU - Hardin, T. C.. AU - Koeller, J. M.. AU - Kuhn, J. G.. AU - Roodman, G. D.. AU - Von Hoff, D. D.. PY - 1993/1/1. Y1 - 1993/1/1. N2 - In conjunction with a Phase I investigation of the antineoplastic activity of recombinant human tumor necrosis factor-α (TNF-α), administered as a 28- day continuous infusion, selected nutritional parameters were evaluated to identify any effect that might be attributed to the TNF infusion. Seven clinically stable men with a variety of tumor types were studied. None had clinical or laboratory evidence of significant malnutrition before entry into the study. Five patients received 10 μg of recombinant human TNF-α per square meter per day and two patients received 25 μg/m2 per day. Indirect calorimetry assessment of resting energy expenditure, body weight, serum TNF concentration, and laboratory analysis of common nutritional markers ...
Effect of Tumor Necrosis Factor-Alpha Inhibitors on Glycemic Control in Patients with Type II Diabetes - P Deepak Udayakumar M.D.
The combination of tumour necrosis factor-alpha-308A and interleukin-10-1082G gene polymorphisms and increased serum levels of related cytokines: susceptibility to vitiligo ...
Oxidative Medicine and Cellular Longevity is a unique peer-reviewed, Open Access journal that publishes original research and review articles dealing with the cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, metabolism, cellular survival and cellular longevity. Oxidative stress impacts almost all acute and chronic progressive disorders and on a cellular basis is intimately linked to aging, cardiovascular disease, cancer, immune function, metabolism and neurodegeneration. The journal fills a significant void in todays scientific literature and serves as an international forum for the scientific community worldwide to translate pioneering
Glutamine attenuates tumor necrosis factor-alpha release and enhances heat shock protein 72 in human peripheral blood mononuclear cells.
A number of recombinant plasmids coding for fusion proteins between human interferon-gamma (IFN-gamma) and human tumour necrosis factor alpha (TNF alpha) or beta (TNF beta) were constructed by using site-directed mutagenesis and ligation of the respective genes. In these proteins the whole IFN-gamma sequence of the molecule is linked at the N terminus via a short polypeptide linker to the TNF alpha sequence lacking two N-terminal amino acid residues or to the whole TNF beta sequence. A series of mutants with deletions in the interferon part of the fusion proteins were also produced. All the fusion genes obtained were efficiently expressed in Escherichia coli under the control of early promoters of bacteriophage T7. The recombinant fusion proteins were found to be unstable inside bacterial cells. Bacterial cell lysates expressing these fusion genes or their deletion mutants showed both biological activities in vitro: the antiviral activity of IFN-gamma and the cytotoxic activity of TNF.
TY - JOUR. T1 - Tumor necrosis factor-α and interleukin-1β production by human fetal Kupffer cells. AU - Kutteh, William H.. AU - Rainey, William E.. AU - Beutler, Bruce. AU - Carr, Bruce R.. PY - 1991/7. Y1 - 1991/7. N2 - This study describes the isolation and characterization of human fetal Kupffer cells. We demonstrated that these cells have the potential to respond to cytokines and lipopolysaccharide with an increased production of tumor necrosis factor-α and interleukin-1β. Kupffer cells were characterized by: (1) morphologic characteristics after adherence to plastic, (2) staining for α-naphthyl acetate esterase, (3) immunofluorescence with monoclonal antibodies, and (4) phagocytosis of latex beads. More than 90% of the adherent cells were identified as macrophages. Kupffer cells cultured with lipopolysaccharide were able to produce interleukin-1β and tumor necrosis factor-α in a time- and dose-dependent fashion and maximal secretion was observed with the use of 10 μg of ...
TNF-alpha is a highly pleiotropic cytokine and plays an important role in regulating HIV-1 replication. It may compromise the integrity of the blood-brain-barrier and, thus, may contribute to the neurotoxicity of HIV-1-infection. Both intravenous drug abuse (IDU) and HIV infection can increase TNF-alpha activity, but little information is available on the effects of a combination of these factors on TNF-alpha. We investigated plasma TNF-alpha levels and mRNA in the peripheral monocytes of 166 men and women in three groups: HIV-1-positive IDUs, HIV-1-negative IDUs, and HIV-negative non-IDU control participants. HIV-1-positive IDUs had higher TNF-alpha levels than HIV-1-negative IDUs who, in turn, had higher levels than controls. TNF-alpha mRNA expression in peripheral monocytes was significantly increased in both HIV-1-positive and negative IDUs compared to controls. These findings show that the effects of HIV infection and intravenous drug use may be additive in increasing TNF-alpha levels. Given the
TY - JOUR. T1 - WISP1, a pro-mitogenic, pro-survival factor, mediates tumor necrosis factor-α (TNF-α)-stimulated cardiac fibroblast proliferation but inhibits TNF-α-induced cardiomyocyte death. AU - Venkatachalam, Kaliyamurthi. AU - Venkatesan, Balachander. AU - Valente, Anthony J.. AU - Melby, Peter. AU - Nandish, Sailesh. AU - Reusch, Jane E B. AU - Clark, Robert A.. AU - Chandrasekar, Bysani. PY - 2009/5/22. Y1 - 2009/5/22. N2 - WNT1-inducible signaling pathway protein-1 (WISP1), a member of the CYR61/CTGF/Nov family of growth factors, can mediate cell growth, transformation, and survival. Previously we demonstrated that WISP1 is up-regulated in post-infarct heart, stimulates cardiac fibroblast proliferation, and is induced by the proinflammatory cytokine tumor necrosis factor-α (TNF-α). Here we investigated (i) the localization of TNF-α and WISP1 in post-infarct heart, (ii) the mechanism of TNF-α-mediated WISP1 induction in primary human cardiac fibroblasts (CF), (iii) the role of ...
BACKGROUND: Because traditional therapies for rheumatoid arthritis (RA) such as methotrexate (MTX) do not produce an adequate response in many patients, newer therapies that block the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) are increasingly being used in combination with MTX.. OBJECTIVE: This study evaluated the efficacy, pharmacokinetics, and safety profile of adalimumab, a fully human anti-TNF alpha monoclonal antibody, when added to continuing MTX therapy.. METHODS: This Phase I, randomized, dose-titration study consisted of a 4-week, double-blind, placebo-controlled treatment phase and a 26-month, open-label continuation phase. Patients with RA who had been taking stable doses of MTX (mean dose, 17 mg/wk) for , or =3 months before enrollment with an inadequate response were randomly assigned to receive 2 single doses of either adalimumab 0.25, 0.5, 1, 3, or 5 mg/kg i.v. or placebo in the double-blind phase. In the open-label phase, patients received treatment with 1 ...
Tumor necrosis factor (TNF) is a cytokine that promotes inflammation and contributes to pathogenesis of inflammatory bowel diseases. Unlike other cells and tissues, intestinal epithelial cells undergo rapid cell death upon exposure to TNF, by unclear mechanisms. We investigated the roles of inhibitor of apoptosis proteins (IAPs) in the regulation of TNF-induced cell death in the intestinal epithelium of mice and intestinal organoids.RNA from cell lines and tissues was analyzed by quantitative polymerase chain reaction, protein levels were analyzed by immunoblot assays. BIRC2 (also called cIAP1) was expressed upon induction from lentiviral vectors in young adult mouse colon (YAMC) cells. YAMC cells, the mouse colon carcinoma cell line MC38, the mouse macrophage cell line RAW 264.7, or mouse and human organoids were incubated with second mitochondrial activator of caspases (Smac)-mimetic compound LCL161 or recombinant TNF-like weak inducer of apoptosis (TNFSF12) along with TNF, and cell death was ...
We describe here a monoclonal antibody (H398) that immunoprecipitates a human 60-kD tumor necrosis factor (TNF) membrane receptor (p60) and competes with TNF binding to p60 but not to p85 TNF receptors. Despite partial inhibition of TNF binding capacity of cells coexpressing both TNF receptor molecules, H398 uniformly and completely inhibits very distinct TNF responses on a variety of cell lines. These data suggest a limited structural heterogeneity in those components actually contributing to TNF responsiveness and identify p60 as a common receptor molecule essential for TNF signal transduction. As H398 is a highly effective TNF antagonist in vitro, it might be useful as a therapeutic agent in the treatment of TNF-mediated acute toxicity. ...
Results: We observed no significant differences in tumour necrosis factor-alpha serum levels between the study groups. In the patient group, an increase in the tumour necrosis factor-alpha serum levels in patients carrying the tumour necrosis factor-alpha (-308 G/A) A allele compared to those without the A allele was found to be statistically significant. Additionally, an increase in the tumour necrosis factor-alpha serum levels in patients carrying tumour necrosis factor-alpha (-308 G/A) AA genotype compared with patients carrying the AG or GG genotypes was statistically significant. No significant differences were found in these 2 polymorphisms between the patient and control groups (p,0.05 ...
TY - JOUR. T1 - Interleukin‐1 and tumor necrosis factor production by tumor‐associated mononuclear leukocytes and peripheral mononuclear leukocytes in cancer patients. AU - Economou, James S.. AU - Colquhoun, Steven D. AU - Anderson, Timothy M.. AU - McBride, William W.. AU - Golub, Sidney. AU - Holmes, E. Carmack. AU - Morton, Donald L.. PY - 1988/1/1. Y1 - 1988/1/1. N2 - The production of interleukin‐I (IL‐I) and tumor necrosis factor (TNF) by tumor‐associated mononuclear leukocytes (TAML) and peripheral mononuclear leukocytes (PBML) from 9 otherwise untreated patients with a variety of malignancies (lung, sarcoma, stomach, renal) was assessed. Cells were cultured for 24 hr in vitro in the presence or absence of lipopolysaccharide (LPS), and IL‐I and TNF levels were measured in culture supernatants. TNF production was comparable between TAMLs and PBMLs. However, a striking defect in IL‐I production by TAMLs was noted. There was no basal production of IL‐I and LPS‐stimulated ...
TY - JOUR. T1 - An inducible autocrine cascade regulates rat hepatocyte proliferation and apoptosis responses to tumor necrosis factor-α. AU - Cosgrove, Benjamin D.. AU - Cheng, Connie. AU - Pritchard, Justin R.. AU - Stolz, Donna B.. AU - Lauffenburger, Douglas A.. AU - Griffith, Linda G.. PY - 2008/7/1. Y1 - 2008/7/1. N2 - Tumor necrosis factor-α (TNF) is an inflammatory cytokine that induces context-dependent proliferation, survival, and apoptosis responses in hepatocytes. TNF stimulates and enhances growth factor-mediated hepatocyte proliferation and survival following partial hepatectomy, but also acts in concert with other inflammatory cytokines of the innate immune response during viral infection to induce apoptosis in hepatocytes. In other epithelial cell types, TNF has recently been shown to stimulate autocrine release of transforming growth factor-α (TGF-α) and interleukin-1 (IL-1) family ligands. Here, we examine the role of these autocrine ligands in modulating TNF-induced ...
Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture. 40% inhibition occurs at the clinically achievable dose of the drug of 1 micrograms/ml. In contrast, the amount of total protein and individual proteins labeled with [35S]methionine and expressed on SDS-PAGE are not influenced. The amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony-stimulating factor produced by monocytes remain unaltered. The selectivity of this drug may be useful in determining the role of TNF-alpha in vivo and modulating its toxic effects in a clinical setting. ...
TY - JOUR. T1 - Associations between tumor necrosis factor-α polymorphisms and susceptibility to pulmonary tuberculosis. T2 - Meta-analysis. AU - Lee, Young Ho. AU - Song, Gwan Gyu. PY - 2015/7/31. Y1 - 2015/7/31. N2 - The aim of this study was to determine whether tumor necrosis factor-α (TNF-α) polymorphisms are associated with susceptibility to pulmonary tuberculosis (PTB) in different ethnic populations. MEDLINE and Embase databases and manual searches were employed to identify articles in which TNF-α polymorphisms were determined in patients with PTB and controls. A meta-analysis was conducted on the associations of the TNF-α -308A/G, -238A/G, and -857T/C polymorphisms with PTB susceptibility. A total of 13 studies met the inclusion criteria, including 12, 6, and 4 studies on TNF-α-308A/G, -238A/G, and -857T/C polymorphisms, respectively. Meta-analysis showed no association between the TNF-α -308A allele and PTB susceptibility in all study subjects (odds ratio, OR = 1.182, 95%CI = ...
TY - JOUR. T1 - Placental tumor necrosis factor-α protein expression during normal human gestation. AU - Basu, Jayasri. AU - Agamasu, Enyonam. AU - Bendek, Bolek. AU - Salafia, Carolyn M.. AU - Mishra, Aruna. AU - Benfield, Nerys C.. AU - Prasad, Priya. AU - Mikhail, Magdy. PY - 2016/3/14. Y1 - 2016/3/14. N2 - Objective: Placental tumor necrosis factor-α (TNF-α) is a cell signaling protein. During pregnancy, TNF-α induces synthesis of matrix metalloproteinases (MMPs) which allows cytotrophoblasts to reach the spiral arteries deeper within the uterine decidua. TNF-α also augments apoptosis of vascular smooth muscle cells surrounding these arteries. In this study, chorionic villi TNF-α protein expression throughout normal human gestation were investigated. Methods: Placental chorionic villi tissues obtained from elective surgical terminations of pregnancy and from uncomplicated term births were assayed using EIA kits (Cayman Chemicals, Ann Arbor, MI, Item # 589201). Results: The median, 25th ...
Transcriptional activity of tumor necrosis factor-alpha gene in peripheral blood mononuclear cells in patients with coronary slow flow
The anti-tumor activity of recombinant human tumor necrosis factor (rHTNF) was examined against four newly induced murine sarcomas (MCA-101, -102, -105, and -106) and a murine adenocarcinoma (MCA-38) transplanted s.c. into C57BL/6 mice. The serum half-life after a single i.v. injection of rHTNF was determined to be 30 +/- 2 min. Tumor-bearing mice were more susceptible to the toxic side effects of rHTNF than were normal mice. Forty-eight percent (41/86) of tumor bearing animals that received 10 micrograms rHTNF died within 48 hr after treatment compared with no deaths in 28 normal animals receiving this dose. Treatment of mice bearing either the MCA-101, -102, -105, or -106 sarcoma or the MCA-38 adenocarcinoma with rHTNF resulted in a marked necrosis of the central portion of each tumor within 24 hr. Animals bearing the weakly immunogenic tumors MCA-105, -106, and -38 experienced a reduction in average tumor area of 47% +/- 5, 46% +/- 6, and 37% +/- 11, respectively, by 3 to 4 days after ...
TY - JOUR. T1 - Dermatologists awareness of and screening practices for hepatitis B virus infection before initiating tumor necrosis factor-α inhibitor therapy. AU - Stine, Jonathan. AU - Bass, Michael. AU - Ibrahim, Dalia. AU - Khokhar, Omar S.. AU - Lewis, James H.. PY - 2011/12/1. Y1 - 2011/12/1. N2 - OBJECTIVE: The aim of the study was to assess dermatologists awareness of available guidelines and drug package insert information on the screening for and management of hepatitis B (HBV) infection in patients receiving tumor necrosis factor-α inhibitor (TNF-αI) drug therapies for dermatological disorders. MATERIALS AND METHODS: An electronic descriptive cross-sectional questionnaire was administered to a random, nationwide sample of physician members of the American Academy of Dermatology. Each participating physician answered 8 questions regarding his or her awareness of the risk of HBV reactivation. RESULTS: More than half of the dermatologists surveyed (52%) were aware of guidelines ...
Tumor necrosis factor-alpha is released from cells by a proteolytic cleavage. Previous work suggested that a specific, non-matrix metalloproteinase carries out this cleavage, but matrix metalloproteinases have also been implicated. In this paper, we report that none of the matrix metalloproteinases tested cleaved peptide substrates as specifically as the non-matrix metalloproteinase. A matrix metalloproteinase did process tumor necrosis factor-alpha extracted from COS cells, but neither tissue inhibitor of metalloproteinases-1 nor -2 blocked tumor necrosis factor-alpha processing by human monocytes. Moreover, tissue inhibitor of metalloproteinases-1 had at most a partial effect on the in vivo release of the cytokine in mice. We conclude that a non-matrix metalloproteinase is the major physiological tumor necrosis factor-alpha convertase.
Mutations in MECP2 cause Rett syndrome, a severe neurological disorder with autism-like features. Duplication of MECP2 also causes severe neuropathology. Both diseases display immunological abnormalities that suggest a role for MeCP2 in controlling immune and inflammatory responses. Here, we used mecp2-null zebrafish to study the potential function of Mecp2 as an immunological regulator. Mecp2-deficiency resulted in an increase in neutrophil infiltration and upregulated expression of the pro- and anti-inflammatory cytokines Il1b and Il10 as a secondary response to disturbances in tissue homeostasis. In contrast, expression of the pro-inflammatory cytokine tumor necrosis factor alpha (Tnfa) was consistently downregulated in mecp2--null animals during development, representing the earliest developmental phenotype described for MeCP2-deficiency to date. Expression of tnfa was unresponsive to inflammatory stimulation, and was partially restored by re-expression of functional mecp2. Thus, Mecp2 is ...
AIM Behcets disease (BD) is a systemic immunoinflammatory disorder and the aetiopathogenesis is to be specified. Cytokines play a role in immune response and in many inflammatory diseases. The aim of this case-control study is to investigate serum pro-inflammatory cytokine tumour necrosis factor (TNF)-alpha, interleukin-1beta (IL-1beta), soluble IL-2 receptor (sIL-2R), IL-6, and chemokine IL-8 levels in patients with BD. We also determined the end product of lipid peroxidation (malondialdehyde (MDA)) in BD patients as an index for oxidative stress. ...
In many different cell types, pro-inflammatory agonists induce the expression of cyclooxygenase 2 (COX-2), an enzyme that catalyzes rate-limiting steps in the conversion of arachidonic acid to a variety of lipid signaling molecules, including prostaglandin E₂ (PGE₂). PGE₂ has key roles in many early inflammatory events, such as the changes of vascular function that promote or facilitate leukocyte recruitment to sites of inflammation. Depending on context, it also exerts many important anti-inflammatory effects, for example increasing the expression of the anti-inflammatory cytokine interleukin 10 (IL-10), and decreasing that of the pro-inflammatory cytokine tumor necrosis factor (TNF). The tight control of both biosynthesis of, and cellular responses to, PGE₂ are critical for the precise orchestration of the initiation and resolution of inflammatory responses. Here we describe evidence of a negative feedback loop, in which PGE₂ augments the expression of dual specificity phosphatase 1, ...
TY - JOUR. T1 - Tumor necrosis factor-α-induced caspase activation mediates endotoxin-related cardiac dysfunction. AU - Carlson, Deborah L.. AU - Willis, Monte. AU - White, D. Jean. AU - Norton, Jureta W.. AU - Giroir, Brett P.. PY - 2005/5/1. Y1 - 2005/5/1. N2 - Objective: Sepsis-induced cardiac dysfunction is a serious clinical syndrome characterized by hypotension, decreased systemic vascular resistance, and elevated cardiac index. Although cytokines such as tumor necrosis factor (TNF)-α have been shown to play a significant role early in this response, the downstream effects of TNF-α signaling on cardiac function, specifically its relationship to apoptosis, have not been fully elucidated. Design: Previous studies from our laboratory have identified endotoxin-induced apoptosis in cardiac cells in vitro. To further determine the role of lipopolysaccharide-induced apoptosis in vivo, mice were injected intraperitoneally with lipopolysaccharide (4 mg/kg), and cardiac apoptosis was detected and ...
Clinical trial for Rheumatoid Arthritis , Safety Study Of Tofacitinib Versus Tumor Necrosis Factor (TNF) Inhibitor In Subjects With Rheumatoid Arthritis
The IUPHAR/BPS Guide to Pharmacology. OX40 - Tumour necrosis factor (TNF) receptor family. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
Blocking the proinflammatory cytokine tumor necrosis factor-alpha failed to stop overall structural progression of hand osteoarthritis, a randomized trial found.
If patients could recognise themselves, or anyone else could recognise a patient from your description, please obtain the patients written consent to publication and send them to the editorial office before submitting your response [Patient consent forms] ...
Introduction In 2008, the Food and Drugs Administration required manufacturers of TNFα antagonists to strengthen their warnings about the risk of serious fungal infections in patients with rheumatoid...
Title:Insulin-Sensiting Effects of Tumor Necrosis Factor Alpha Inhibitors in Rheumatoid Arthritis: A Systematic Review and Meta-Analysis. VOLUME: 13 ISSUE: 3. Author(s):Christian Leporini*, Emilio Russo, Salvatore D`Angelo, Franco Arturi, Giovanni Tripepi, Rosario Peluso, Rosa Daniela Grembiale, Ignazio Olivieri, Giovambattista De Sarro and Francesco Ursini. Affiliation:Department of Health Sciences, University of Catanzaro , Department of Health Sciences, University of Catanzaro , Rheumatology Department of Lucania, San Carlo Hospital of Potenza and Madonna delle Grazie Hospital of Matera, Potenza, Department of Health Sciences, University of Catanzaro , CNRIBIM, National Research Council-Institute of Biomedicine, Reggio Calabria, Department of Clinical Medicine and Surgery - Rheumatology Research Unit - Federico II University, Naples, Department of Health Sciences, University of Catanzaro , Rheumatology Department of Lucania, San Carlo Hospital of Potenza and Madonna delle Grazie Hospital of ...
T cell receptor (TCR)-dependent regulatory T cell (Treg) activity controls effector T cell (Teff) function and is inhibited by the inflammatory cytokine tumor necrosis factor-α (TNF-α). Protein kinase C-θ (PKC-θ) recruitment to the immunological synapse is required for full Teff activation. In contrast, PKC-θ was sequestered away from the Treg immunological synapse. Furthermore, PKC-θ blockade enhanced Treg function, demonstrating PKC-θ inhibits Treg-mediated suppression. Inhibition of PKC-θ protected Treg from inactivation by TNF-α, restored activity of defective Treg from rheumatoid arthritis patients, and enhanced protection of mice from inflammatory colitis. Treg freed of PKC-θ-mediated inhibition can function in the presence of inflammatory cytokines and thus have therapeutic potential in control of inflammatory diseases.. ...
Mouse Monoclonal Tumor Necrosis Factor antibody for FACS. Published in 7 Pubmed References. Order this anti-Tumor Necrosis Factor antibody. | Product number ABIN4898910
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Data on interleukin-6 (IL-6) and tumour necrosis factor-a (TNF-a) release during acute exercise are not conclusive, and information is lacking about the impact of physical inactivity. Some studies have shown an increase, but others report no changes in IL-6 and TNF-a release during exercise. We have now studied the temporal relationship of leg IL-6 and TNF-a release before and during isolated two-legged exercise after 14 days of one-leg immobilization (IM) while the other leg served as the control (CON) leg. Fifteen healthy male subjects (mean ± SEM age, 23 ± 1 years; body mass index, 23.6 ± 0.7 kg m; and maximal oxygen uptake, 46.8 ± 1.4 ml kg min) performed 45 min of two-legged dynamic knee-extensor exercise at 19.6 ± 0.8 W. Arterial and femoral venous blood samples from the CON and the IM leg were collected every 15 min during exercise, and leg blood flow was measured with Doppler ultrasound. The arterial plasma IL-6 concentration increased (P ,0.05) with exercise (rest, 1.3 ± 0.1 pg ...
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Exposure of the airways to air toxins initiates transient and reversible airway injury to both adults and young children. Repetitive exposures of children residing within high oxidant communities leads to impairment of lung growth and pulmonary function, and remodeling of airway epithelial tissues is also suggested to occur. In the completely normal/healthy airway, exposure to ozone (O3), a ubiquitous urban air pollutant, induces an inflammatory response that is characterized by increases in epithelial permeability, neutrophilic infiltration, and bronchial hyperreactivity. Inhalation by humans of the pleiotropic pro-inflammatory cytokine tumor necrosis factor (Tnf) leads to the development of nearly identical responses: hyperresponsiveness of the bronchial airway (AHR), and neutrophil influx. Using controlled exposure to O3 in a laboratory setting, we have recently established a link between a genetic single nucleotide polymorphism (SNP) of TNF gene (-308) and the development of AHR to ...
Exposure of the airways to air toxins initiates transient and reversible airway injury to both adults and young children. Repetitive exposures of children residing within high oxidant communities leads to impairment of lung growth and pulmonary function, and remodeling of airway epithelial tissues is also suggested to occur. In the completely normal/healthy airway, exposure to ozone (O3), a ubiquitous urban air pollutant, induces an inflammatory response that is characterized by increases in epithelial permeability, neutrophilic infiltration, and bronchial hyperreactivity. Inhalation by humans of the pleiotropic pro-inflammatory cytokine tumor necrosis factor (Tnf) leads to the development of nearly identical responses: hyperresponsiveness of the bronchial airway (AHR), and neutrophil influx. Using controlled exposure to O3 in a laboratory setting, we have recently established a link between a genetic single nucleotide polymorphism (SNP) of TNF gene (-308) and the development of AHR to ...
The present invention relates to ligands which bind to human tumor necrosis factor alpha (TNF) in a manner such that upon binding of these ligands to TNF the biological activity of TNF is modified. In preferred forms the ligand binds to TNF in a manner such that the induction of endothelial procoagulant activity of the TNF is inhibited; the binding of TNF to receptors on endothelial cells is inhibited; the induction of fibrin deposition in the tumor and tumor regression activities of the TNF are enhanced; and the cytotoxicity and receptor binding activities of the TNF are unaffected or enhanced on tumor cells. The ligand is preferably an antibody, F(ab) fragment, single domain antibody (dABs) single chain antibody or a serum binding protein. It is preferred, however, that the ligand is a monoclonal antibody or F(ab) fragment thereof.
The team reported that 96 had indeterminate colitis from the Cambridge/Eastern panel in the United Kingdom.. The research team also included 760 healthy control subjects.. The team assessed DLG5_113G/A, DLG5_4136C/A, tumor necrosis factor-857C/T, and tumor necrosis factor-1031T/C polymorphisms.. Known Crohns disease-predisposing variants in CARD15/NOD2 were also genotyped to permit analysis for reported epistatic interactions.. Tumor necrosis factor-857 was shown to be associated with IBD overall.. A formal interaction test showed that tumor necrosis factor-857 is associated equally with ulcerative colitis and Crohns disease.. The research team found that neither of the DLG5 alleles, however, was associated with IBD.. Subgroup analysis also failed to show evidence of association between either DLG5 allele or genotype frequencies and ulcerative colitis or Crohns disease.. Stratification of tumor necrosis factor-alpha and DLG5 cases by CARD15 genotype made no significant difference in the ...
TY - JOUR. T1 - Tumor-nekrose-faktor alpha bei chronischer herzinsuffizienz. Klinische manifestation und therapeutische möglichkeiten. AU - Genth-Zotz, Sabine. AU - Bolger, Aidan P.. AU - Anker, Stefan D.. PY - 2001. Y1 - 2001. N2 - Background: Chronic heart failure (CHF) may be seen as a multi-system disorder with its origin in the heart but including many extracardiac manifestations. Immunological abnormalities are recognized in this context, in particular, changes in the expression of mediators of the innate immune response. Importance of TNF: Higher levels of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF) are found in the circulation and in the myocardium of patients with chronic heart failure than in controls. TNF has been implicated in a number of pathophysiological processes that are thought to be important to the progression of chronic heart failure. Therapies directed against this cytokine might therefore represent anovel approach to heart failure management.. AB - ...
Effects of Tumor Necrosis Factor-a on Insulin Stimulated Amino Acid Transport in Cultured Rat Hepatocytes. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
While monoclonal antibodies against tumor necrosis factor-α (TNFα) are effective in treating Crohns disease (CD), approximately one-third