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. ...
TY - JOUR. T1 - Endogenous tumor necrosis factor (TNF) production and modification of pathological lesions in experimental Escherichia coli endotoxemia of piglets. AU - Nakajima, Yasuyuki. AU - Momotani, Eiichi. AU - Takahashi, Hideyuki. AU - Ishikawa, Yoshiharu. AU - Ito, Takashi. AU - Kanesaki, Makoto. AU - Madarame, Hiroo. PY - 1995/1/1. Y1 - 1995/1/1. N2 - We examined the kinetics of tumor necrosis factor (TNF) production induced by Escherichia coli lipopolysaccharide (LPS) in relation to LPS tolerance and endotoxemic lesions of piglets. The plasma of piglets demonstrated cytotoxicity to TNF-sensitive L929 cells between 0.5 and 4 h after inoculation with 200 μg kg -1 of LPS. This cytotoxicity was neutralized by anti-bovine TNF serum. These piglets had disseminated intravascular coagulation (DIC) and meningoencephalitis. However, if piglets were first treated with three doses of 40 μg kg -1 of LPS, both TNF production and the occurrence of DIC were inhibited when 200 μg kg -1 of LPS was ...
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 ...
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 - 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 ...
Tumor Necrosis Factor (TNF) Inhibitor Drugs Industry Outlook 2021 The outbreak of covid-19 in the global market has made companies uncertain about their future scenario as the prolonged lock-down finds a serious economic slump. The latest survey on COVID-19 Outbreak-Global Tumor Necrosis Factor (TNF) Inhibitor Drugs Market is conducted to provide hidden gems performance analysis. Essential growth factors and study of Basis points [BPS] have been discussed in the following report. Research Report explains a detailed overview of market dynamics, segmentation, product portfolio, business plans, and the latest development in the industry.. Staying on top of market trends & drivers is crucial for decision-makers to hold this emerging opportunity. The study provides information on market trends and development, drivers, capacities, technologies, and the changing investment structure of the Tumor Necrosis Factor (TNF) Inhibitor Drugs market. The development scope, feasibility study, Tumor Necrosis ...
TY - JOUR. T1 - In vitro and in vivo inhibition of LPS-induced tumor necrosis factor-α production by dimeric gallotannin analogues. AU - Feldman, Ken S.. AU - Wilson, Sarah L.. AU - Lawlor, Michael D.. AU - Lang, Charles H.. AU - Scheuchenzuber, William J.. PY - 2002/1/1. Y1 - 2002/1/1. N2 - Designed dimeric gallotannin analogues featuring two tetragalloylglucopyranose cores connected by various hydrocarbon linkers inhibit tumor necrosis factor-α secretion from lipopolysaccharide-stimulated human peripheral blood mononuclear cells by up to 53% (5-24 μM concentration range) compared to control. Comparable suppression of tumor necrosis factor-α levels (∼50% vs control) was observed in the plasma of rats co-treated with lipopolysaccharide and specific tannin analogues selected for their lack of interleukin 1-β stimulating activity.. AB - Designed dimeric gallotannin analogues featuring two tetragalloylglucopyranose cores connected by various hydrocarbon linkers inhibit tumor necrosis ...
TY - JOUR. T1 - Zinc attenuates tumor necrosis factor-mediated activation of transcription factors in endothelial cells. AU - Connell, Patrice. AU - Young, Valerie M.. AU - Toborek, Michal. AU - Cohen, Donald A.. AU - Barve, Shirish. AU - McClain, Craig J.. AU - Hennig, Bernhard. PY - 1997/10/1. Y1 - 1997/10/1. N2 - Objective: The objective of the study was to test the hypothesis that zinc can protect against endothelial dysfunction by interfering with oxidative stress-mediated cellular signaling and subsequent inhibition of an endothelial cell inflammatory response. Our approach was to compare alterations on molecular and biochemical levels with changes in endothelial barrier function that occur in zinc deficient conditions. Methods: To investigate our hypothesis, endothelial cells were exposed to zinc deficient media for 2 to 10 days to deplete cellular zinc stores. Following this, half of the groups received zinc supplementation (9.2 2μM) for 48 hours. The other half served as zinc deficient ...
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
TY - JOUR. T1 - Murine tumour necrosis factor plays a protective role during the initial phase of the experimental infection with Trypanosoma brucei brucei. AU - MAGEZ, STEFAN. AU - LUCAS, RUDOLF. AU - DARJI, AYUB. AU - SONGA, EMMANUEL BAJYANA. AU - HAMERS, RAYMOND. AU - BAETSELIER, PATRICK DE. PY - 1993/11. Y1 - 1993/11. N2 - Soluble extracts from salivarian trypanosomes (Trypanosoma brucei brucei, T. evansi and T. congolense) were shown to be capable of inducing murine tumour necrosis factor (mTNF) secretion, both in vivo and in vitro, whereas the soluble extract of an intracellular trypanosome (T. cruzi) failed to do so. Furthermore, the role of mTNF during the initial phase of experimental infections with T. brucei was studied by treating infected mice with mTNF‐inducing trypanosoma soluble extract and with neutralizing monoclonal anti‐mTNF antibodies. Treatment of the infected animals with different doses of T. brucei soluble extract resulted in a lower first parasitaemia peak (low ...
Glutamine attenuates tumor necrosis factor-alpha release and enhances heat shock protein 72 in human peripheral blood mononuclear cells.
The adaptor molecule Lnk negatively regulates tumor necrosis factor-alpha-dependent VCAM-1 expression in endothelial cells through inhibition of the ERK1 and -2 pathways. J Biol Chem. 2006 Jul 21; 281(29):20148-59 ...
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.
Background: The tumor necrosis factor alpha (TNFα) is a cytokine that produced principally by monocyte/macrophages and T lymphocytes, respectively. TNFα is recognized as the primary mediator of immunity in inflammation reaction. One important application of Tumor Necrosis Factor Receptor 2 (TNFR2) is for the treatment of autoimmune diseases like rheumatoid arthritis (RA). Objectives: The aim of this study is to examine the therapeutic trace of the recombinant humanTNFR2 on collagen-induced arthritis (CIA) in mice. Materials and Methods: CIA was created in 20 mice by immunization with bovine type II collagen (CII). After the mice were boosted on day 21, they were injected with the recombinant protein in test group (1 mg.kg-1) and assessed edema in paws and knee joints after two weeks. The quantities of inflammatory cytokines such as TNF-α, interleukin-1 beta (IL-β1), interleukin-6 (IL-6), and interleukin-10(IL-10) in serum were evaluated through enzyme-linked immunosorbent assay (ELISA) kit. In
Tumor necrosis factor alpha (TNF-alpha) is a cytokine that belongs to the tumor necrosis factor (TNF) superfamily. TNF-alpha is mainly secreted by macrophages. TNF-alpha is involved in the regulat...
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 ...
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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 ...
Tumor necrosis factor (TNF) alpha has been shown to be a major therapeutic target in rheumatoid arthritis with the success of anti-TNFalpha antibody clinical trials. Although signaling pathways leading to TNFalpha expression have been studied in some detail, there is evidence for considerable differences between individual cell types. This prompted us to investigate the intracellular signaling pathways that result in increased TNFalpha synthesis from macrophages in the diseased synovial joint tissue. Using an adenoviral system in vitro we report the successful delivery of genes to more than 95% of normal human macrophages. This permitted us to show, by using adenoviral transfer of IkappaB alpha, the natural inhibitor of NF-kappaB, that induction of TNFalpha in normal human macrophages by lipopolysaccharide, but not by some other stimuli, was inhibited by 80%. Furthermore the spontaneous production of TNFalpha from human rheumatoid joint cell cultures was inhibited by 75%, indicating that the NF-kappaB
Previous studies in the laboratory have shown that the pro-inflammatory cytokine tumor necrosis factor (TNF)-alpha plays a pivotal role in the pathogenesis of rheumatoid arthritis (RA). The mechanisms involved in regulating monocyte/macrophage cytokine production are not yet fully understood, but are thought to involve both soluble factors and cell/cell contact with other cell types. We and others have previously demonstrated that T cells activated through the T cell receptor/CD3 complex induce monocyte TNF-alpha production by contact-mediated signals. In this report, we investigated further whether T cells activated by cytokines in the absence of T cell receptor stimulation also regulate monocyte cytokine production. T cells were activated in an antigen-independent manner using the cytokines interleukin (IL)-15 or IL-2 alone, or in combination with IL-6 and TNF-alpha. Subsequently, T cells were fixed and incubated with monocytes. Fixed, cytokine-stimulated T cells induced monocytes to secrete TNF-alpha
TNF-alpha increases the local estrogen biosynthesis in human endometrial glandular cells and directs estrogen metabolism into more hormonally active and carcinogenic metabolites. These effects may impact many physiological and pathological processes that occur within the endometrium.
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. ...
A B Millar, R F Miller, N M Foley, G A W Rook, S J G Semple; Tumour Necrosis Factor (Tnf Alpha) Production by Peripheral Blood Monocytes and Alveolar Macrophages from Patients with Hiv-Related Lung Disease. Clin Sci (Lond) 1 January 1990; 78 (s22): 17P. doi: https://doi.org/10.1042/cs078017P. Download citation file:. ...
TY - JOUR. T1 - Tumour necrosis factor-a induces hyperreactivity in tracheal smooth muscle of the guinea-pig in vitro.. AU - Pennings, H.J.. AU - Kramer, K.. AU - Bast, A.. AU - Buurman, W.A.. AU - Wouters, E.F.M.. PY - 1998. Y1 - 1998. N2 - Recent studies have implicated a role for tumour necrosis factor-α (TNFα) in the development of the asthmatic reaction. In this study, we examined the influence of TNFα on isotonic contraction of tracheal smooth muscle of the guinea-pig in vitro in response to methacholine. Tracheal rings were incubated with recombinant human (rh)TNFα (3x10. AB - Recent studies have implicated a role for tumour necrosis factor-α (TNFα) in the development of the asthmatic reaction. In this study, we examined the influence of TNFα on isotonic contraction of tracheal smooth muscle of the guinea-pig in vitro in response to methacholine. Tracheal rings were incubated with recombinant human (rh)TNFα (3x10. U2 - 10.1183/09031936.98.12010045. DO - ...
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 ...
TY - JOUR. T1 - Effects of tumor necrosis factor-α on the synthesis of DNA, the secretion of matrix metalloproteinases/tissue inhibitors of metalloproteinases, and the activity of invasive migration in cultured vascular smooth muscle cells. AU - Kaji, Toshiyuki. AU - Hiraga, Shouichi. AU - Yamamoto, Chika. AU - Fujiwara, Yasuyuki. AU - Ueda, Yoshimichi. AU - Zisaki, Fumiko. AU - Iwata, Kazushi. AU - Okada, Yasunori. AU - Katsuda, Shogo. PY - 2002/8. Y1 - 2002/8. N2 - To address the question of whether or not tumor necrosis factor-α (TNF-α) regulates the functions of vascular smooth muscle cells (SMCs), dense or sparse cultures of the cells derived from human aorta were treated with TNF-α or TNF-α neutralizing antibody (TNF-α Ab). The incorporation of [3H]thymidine into the acid-insoluble fraction of SMCs was significantly inhibited by TNF-α, but stimulated by TNF-α Ab only when the cells had a high cell density. TNF-α significantly increased the accumulation of matrix ...
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. ...
Distributions of tumor necrosis factor (TNF) and its soluble receptor forms, R55-BP and R75-BP, were analyzed in the cerebrospinal fluid of patients with severe acute or chronic central nervous system infections. Tuberculous infections were associated with high ratios of R55-BP and R75-BP to TNF, 27.2 and 28.0, respectively, suggesting a small biologically active fraction of TNF. The opposite was found in subjects with acute bacterial meningitis. They had large fractions of biologically active TNF and thus low ratios of R55-BP and R75-BP to TNF, 3.7 and 4.0, respectively. It is hypothesized that chronic infectious diseases, such as tuberculous infections, may be associated with inadequate production of TNF and a concomitant relative increase of soluble TNF receptors, which may prolong the disease ...
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 ...
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.
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 ...
TY - JOUR. T1 - Nitric oxide modulates interleukin-1β and tumour necrosis factor-α synthesis, and disease regression by alveolar macrophages in pulmonary tuberculosis. AU - Wang, Chun Hua. AU - Kuo, Han Pin. PY - 2001/5/9. Y1 - 2001/5/9. N2 - Pretreatment with nitric oxide synthase (NOS) inhibitors profoundly increases mortality, bacterial burden and pathological tissue damage in mice infected with Mycobacterium tuberculosis. Nitric oxide (NO) production is enhanced in alveolar macrophages (AM) of tuberculosis (TB) patients. Interleukin (IL)-1β and tumour necrosis factor (TNF)-α released from AM are involved in the immune response to mycobacterial infection. The aim of the present study was to examine whether NO is implicated in IL-1β and TNF-α synthesis by AM and related to the resolution of disease activity in TB patients. Purified AM were retrieved by bronchoalveolar lavage from TB patients and normal subjects, and cultured in the presence or absence of a NO inhibitor, ...
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 - A novel tumor necrosis factor-mediated mechanism of direct epithelial sodium channel activation. AU - Czikora, István. AU - Alli, Abdel. AU - Bao, Hui Fang. AU - Kaftan, David. AU - Sridhar, Supriya. AU - Apell, Hans Jürgen. AU - Gorshkov, Boris. AU - White, Richard. AU - Zimmermann, Astrid. AU - Wendel, Albrecht. AU - Pauly-Evers, Meike. AU - Hamacher, Jürg. AU - Garcia-Gabay, Irène. AU - Fischer, Bernhard. AU - Verin, Alexander. AU - Bagi, Zsolt. AU - Pittet, Jean Francois. AU - Shabbir, Waheed. AU - Lemmens-Gruber, Rosa. AU - Chakraborty, Trinad. AU - Lazrak, Ahmed. AU - Matthay, Michael A.. AU - Eaton, Douglas C.. AU - Lucas, Rudolf. PY - 2014/9/1. Y1 - 2014/9/1. N2 - Rationale: Alveolar liquid clearance is regulated by Na+ uptake through the apically expressed epithelial sodium channel (ENaC) and basolaterally localized Na+-K+-ATPase in type II alveolar epithelial cells. Dysfunction of these Na+ transporters during pulmonary inflammation can contribute to pulmonary ...
Phase I trial of recombinant human gamma-interferon and recombinant human tumor necrosis factor in patients with advanced gastrointestinal cancer.
The chromatographic behaviour of recombinant human tumour necrosis factor beta (rhTNF-β) (pI ~9.0) during cation-exchange chromatography at pH 7.5 is investigated. Without prior treatment of the Escherichia coli cell extract with polyethyleneimine (PEI), very little rhTNF-β was bound to the column. However, upon addition of 5% PEI (100 μl ml-1) to the cell lysate, rhTNF-β was shown to bind to cation-exchange columns normally. TNF-β was readily precipitated from the clarified cell extract by 20% ammonium sulphate, but only ca. 25% of this precipitate could be re-solubilized for further purification. However, when 5% PEI was included in the solubilization buffer, the balance of the rhTNF-β could be recovered. It is proposed that charge interaction between rhTNF-β and nucleic acids in the cell extract is responsible for both of these anomalous phenomena, and that PEI (a cationic polyelectrolyte) was able to disrupt this interaction by displacing rhTNF-β from the charge complex ...
Incubation of the human U937 histiocytic lymphoma cell line with granulocyte-macrophage colony stimulating factor (GM-CSF) rendered the cells responsive to induction of TNF by LPS. Treatment with IL-6 reduced TNF production in GM-CSF-primed U937 cells. The inhibitory effect was most pronounced (approximately equal to 80%) when IL-6 was added either along with GM-CSF or within the first 3 h of GM-CSF treatment. Both GM-CSF or IL-6 inhibited [3H]TdR uptake in U937 cells, and simultaneous treatment with GM-CSF and IL-6 resulted in an additive inhibitory effect on cell proliferation. However, the inhibition of TNF production could not be explained by the inhibitory effect of IL-6 on cell growth, nor was it due to a reduction in cell viability. An inhibition of TNF production by IL-6 was also demonstrated in cultured human peripheral blood monocytes. Treatment with IL-6 also resulted in a dose-dependent reduction of the 17-kDa TNF band revealed by SDS-PAGE after labeling monocytes with [35S]cysteine ...
Looking for online definition of tumor necrosis factor-alpha (alpha) in the Medical Dictionary? tumor necrosis factor-alpha (alpha) explanation free. What is tumor necrosis factor-alpha (alpha)? Meaning of tumor necrosis factor-alpha (alpha) medical term. What does tumor necrosis factor-alpha (alpha) mean?
Tumor necrosis factor (TNF) and interferon gamma (IFN-gamma) are pluripotent cytokines and have multiple functions during the inflammatory response. Using a murine model of autoimmune myocarditis, we studied the role of TNF and IFN-gamma in myocardial inflammation. Neutralizing monoclonal antibodies against TNF-alpha/beta and IFN-gamma were administered to myosin-immunized A/J mice to assess the effect on the severity of myocardial inflammation. Anti-TNF treatment significantly reduced the severity of myocarditis compared with rat immunoglobulin G or saline controls (p less than 0.0007) when given before myosin immunization. Myosin-specific lymph node T-cell proliferation studies showed no difference in the proliferative response between the anti-TNF-treated mice and controls. Administration of anti-TNF to mice after myosin immunization had no effect on the severity of inflammation. This suggests that TNF is an important mediator early in the pathogenesis of myocardial inflammation in this model ...
TY - JOUR. T1 - Tumor necrosis factor-α is not essential in endotoxin induced eye inflammation. T2 - Studies in cytokine receptor deficient mice. AU - Rosenbaum, James T.. AU - Han, Young Bok. AU - Park, Jong Moon. AU - Kennedy, Michael. AU - Planck, Stephen R.. N1 - Copyright: Copyright 2007 Elsevier B.V., All rights reserved.. PY - 1998/12. Y1 - 1998/12. N2 - Objective. Anterior uveitis frequently occurs in association with specific systemic inflammatory diseases. Interleukin 1 (IL-1) and tumor necrosis factor-α (TNF-α) have been implicated in the pathogenesis of these diseases. We evaluate the need for these cytokines in a model of anterior uveitis. Methods. Endotoxin was injected into the vitreous of mice deficient in IL-1 receptor type I, TNF receptors p55 and p75, both IL-1R1 and TNFR p55, or controls. Eyes were harvested after 24 h for histology and IL-6 bioassays or after 3 h for reverse transcriptase-polymerase chain reaction analysis of mRNA for specific cytokines or enzymes. ...
TY - JOUR. T1 - Protective effect of etanercept, an inhibitor of tumor necrosis factor-α, in a rat model of retinal ischemia. AU - Bae, Hyoung Won. AU - Lee, Naeun. AU - Seong, Gong Je. AU - Rho, Seungsoo. AU - Hong, Samin. AU - Kim, Chan Yun. N1 - Publisher Copyright: © 2016 Bae et al.. PY - 2016/6/4. Y1 - 2016/6/4. N2 - Background: To assess the neuroprotective effect of etanercept (Enbrel®) which is a commercialized Tumor necrosis factor-α (TNF-α) inhibitor on axonal injury in an animal model of acute ischemia. Methods: Acute ischemia was induced by intraocular pressure elevation in 36 rats. The treatment groups underwent subcutaneous injection of etanercept (0.3 or 1.0 mg/kg) three times per week up to 4 weeks. The control groups were treated in the same manner using the same volume of phosphate-buffered saline (PBS). Optic nerve damage was evaluated by counting the number of axons under a transmission electron microscope. Microglial cell activity was assessed using Iba1 and CD68. ...
TY - JOUR. T1 - Tumor necrosis factor-α is decreased in the umbilical cord plasma of patients with severe preeclampsia. AU - Kupferminc, Michael J.. AU - Peaceman, Alan M.. AU - Dollberg, Shaul. AU - Socol, Michael L.. PY - 1999/1/1. Y1 - 1999/1/1. N2 - We investigated the role of the fetal immune system in pregnancies complicated by preeclampsia by assessing umbilical cord plasma levels of the cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Nineteen nulliparous patients with severe preeclampsia composed the study group (group A). A comparison group was comprised of 19 healthy nulliparous patients with uneventful pregnancies (group B). Mixed umbilical cord blood was collected immediately after delivery. Plasma was prepared and all samples were assayed for TNF-α and IL-1β by specific enzyme-linked immunoassays (ELISAs). Data are presented as the median with range of values. The length of labor was similar in both groups. TNF-α was detected less frequently in the ...
TY - JOUR. T1 - Comparison of tumor necrosis factor-α effect on the expression of iNOS in macrophage and cardiac myocytes. AU - Sanders, D. Bradford. AU - Larson, Douglas F.. AU - Hunter, Kyler. AU - Gorman, Mark. N1 - Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 2001/1. Y1 - 2001/1. N2 - Proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), are elevated during cardiopulmonary bypass (CPB), heart failure, and inflammatory cardiac and systemic diseases. Elevated TNF-α has been linked to diminished cardiac function, decreased systemic vascular resistance, as well as renal and pulmonary dysfunction. It is understood that myocardial tissues can express TNF-α, which results in the induction of inducible nitric oxide synthase (iNOS) leading to a significant decline in cardiac function and other direct effects. The hypothesis of this study was to determine if TNF-α would stimulate iNOS and its product nitric oxide (NO) similarly in immortalized macrophage ...
TY - JOUR. T1 - Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF). T2 - Similarities between TNF-α and interleukin. AU - Jacob, Chaim O.. AU - Aiso, Sadakazu. AU - Michie, Sara A.. AU - Mcdevitt, Hugh O.. AU - Acha-Orbea, Hans. N1 - Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 1990. Y1 - 1990. N2 - The role of tumor necrosis factor α (TNF-α) in the pathogenesis of autoimmune diabetes mellitus was tested in the nonobese mouse (NOD) model system. The effects of TNF-α were assessed on three levels: (i) insulitis development, (ii) development of overt diabetes, (iii) adoptive transfer of diabetes by splenic lymphocytes. Spontaneous diabetes mellitus was blocked in NOD mice by long-term treatment with recombinant TNF-α. Treatment with TNF-α caused a significant reduction in the lymphocytic infiltration associated with the destruction of the insulin-producing beta cells. Class II major histocompatibility complex la expression by islet cells ...
TY - JOUR. T1 - The inhibition in tumor necrosis factor-α-induced attenuation in endothelial thrombomodulin expression by carvedilol is mediated by nuclear factor-κB and reactive oxygen species. AU - Lin, Pen-Yuan. AU - Shen, Hsi Che. AU - Chen, Chien Jen. AU - Wu, Shu En. AU - Kao, Hsien Li. AU - Huang, Jen-Hung. AU - Wang, Danny Ling. AU - Chen, Shih-Chung. PY - 2010/1. Y1 - 2010/1. N2 - Carvedilol, a nonselective β-adrenoceptor antagonist, has been shown to possess antioxidant effects and reduce the risk of hospitalization and death in patients with severe congestive heart failure, which is featured by the activation of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), and leads to thrombotic complications. Thrombomodulin (TM) plays protective roles against thrombosis. Treatment of ECs with TNF-α resulted in a down-regulation in the TM expression in a time-dependent manner. Pre-treatment of ECs with carvedilol (1 and 10 μM) for 1 h significantly up-regulated the TM ...
TY - JOUR. T1 - Effects of tumor necrosis factor-α on cell proliferation, prostaglandins and matrix-metalloproteinases production in rat endometrial stromal cells cultured in vitro. AU - Gamo, Toru. AU - Yamauchi, Nobuhiko. AU - Nishimura, Kyohei. AU - Watanabe, Ryo. AU - Matsumoto, Kenji. AU - Oozono, Shinji. AU - Kubota, Kaiyu. AU - He, Pei Jian. AU - Soh, Tomoki. AU - Hattori, Masa Aki. PY - 2007/12/1. Y1 - 2007/12/1. N2 - Tumor necrosis factor-α (TNF-α) is known as a pluripotent cell mediator, and it is implicated in the control of uterine cell growth, differentiation and function during estrous cycle and pregnancy. In this study, we investigated the effect of TNF-α on endometrial stromal cells derived from rat uterus (rat endometrial stromal cells, RES). RES were isolated from rat endometrium at day 5 of pregnancy. Proliferation activities of RES were measured by using bromodeoxyuridine (BrdU) labeling kit, the productions of prostaglandin E2 (PGE2) and prostaglandin F2α (PGF 2α) were ...
TY - JOUR. T1 - Tumor necrosis factor-α modulates epithelial mesenchymal transition mediators ZEB2 and S100A4 to promote cholangiocarcinoma progression. AU - Techasen, Anchalee. AU - Namwat, Nisana. AU - Loilome, Watcharin. AU - Duangkumpha, Kassaporn. AU - Puapairoj, Anucha. AU - Saya, Hideyuki. AU - Yongvanit, Puangrat. PY - 2014/9. Y1 - 2014/9. N2 - Background The epithelial-mesenchymal transition (EMT) process strongly contributes to cancer metastasis. This study was to investigate the alteration of EMT-related proteins (ZEB1, ZEB2 and S100A4) in cholangiocarcinoma (CCA) tissues. The effect of tumor necrosis factor-α (TNF-α) on the expression of those molecules in CCA cells was investigated. Methods The quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assay was used to quantify ZEB1, ZEB2 and S100A4 mRNA levels in 50 CCA tissues and related its expression to clinicopathological data. ZEB2 protein immunostaining was investigated in 165 CCA tissues. The effect of ...
TY - JOUR. T1 - Effects of tumor necrosis factor-α on podocyte expression of monocyte chemoattractant protein-1 and in diabetic nephropathy. AU - Chung, Choon Hee. AU - Fan, Jingyi. AU - Lee, Eun Young. AU - Kang, Jeong Suk. AU - Lee, Seung Joo. AU - Pyagay, Petr E.. AU - Khoury, Charbel C.. AU - Yeo, Tet Kin. AU - Khayat, Mark F.. AU - Wang, Amy. AU - Chen, Sheldon. N1 - Publisher Copyright: © 2015 S. Karger AG, Basel.. PY - 2015/1/1. Y1 - 2015/1/1. N2 - Background/Aims: Tumor necrosis factor (TNF)-α is believed to play a role in diabetic kidney disease. This study explores the specific effects of TNF-α with regard to nephropathy-relevant parameters in the podocyte. Methods: Cultured mouse podocytes were treated with recombinant TNF-α and assayed for production of monocyte chemoattractant protein-1 (MCP-1) by enzyme-linked immunosorbent assay (ELISA). TNF-α signaling of MCP-1 was elucidated by antibodies against TNF receptor (TNFR) 1 or TNFR2 or inhibitors of nuclear factor-kappaB ...
In this study, we explore the regulatory roles of pro-inflammatory cytokine tumor necrosis factor alpha (TNF) in the innate immunity of macrophages against B. abortus infection. We show that infection of macrophage with B. abortus induces marked expression and secretion of TNF which subsequently binds to TNF receptor 1 (TNFR-1) and activates a downstream signaling cascade of the innate immunity. Blocking of TNF signaling resulted in a notable increase of B. abortus survival which was associated with an increase of anti-inflammatory cytokine interleukin 10 (IL-10), a beneficial effector of Brucella survival, as well as remarkable decrease of reactive oxygen species (ROS) and nitric oxide (NO), antibrucella molecules ...
TY - JOUR. T1 - Tumor necrosis factor-α develops late anaphylactic reaction through cytosolic phospholipase A2 activation. AU - Kang, Nam In. AU - Kim, Hae Kyoung. AU - Ko, Hyun Mi. AU - Kim, Jae Hong. AU - You, Hye Jin. AU - Choi, Il Whan. AU - Im, Suhn Young. AU - Lee, Hern Ku. PY - 2008/11. Y1 - 2008/11. N2 - Background: We have recently reported that tumor necrosis factor (TNF)-α plays an important role in the development of a late anaphylactic reaction, but the downstream pathway beyond TNF-α remains unclear. Objective: It was the aim of this study to examine whether TNF-α induces late-phase anaphylaxis via the activation of cytosolic phospholipase A 2 (cPLA2). Methods: Using a murine model of active systemic anaphylaxis to penicillin V, the induction of the late phase of anaphylaxis was quantified by measuring the increase in hematocrit value as well as the plasma level of platelet-activating factor in TNF-α knockout mice. Phosphorylation of mitogen-activated protein kinases (MAPKs) ...
TY - JOUR. T1 - Persistent anti-inflammatory cytokine release in septic shock. AU - Sfeir, Tacla. AU - Saha, Dhanonjoy. AU - Astiz, Mark. AU - Rackow, Eric. PY - 1999/1/1. Y1 - 1999/1/1. N2 - Introduction: During septic shock dysregulation of monocyte cytokine release contributes to immunosuppression. We evaluated the difference in release of the pro-inflammatory cytokine tumor necrosis factor (TNF-α) and the anti-inflammatory cytokine interleukin 10 (IL-10) from blood monocytes isolated from healthy individuals and septic shock patients. Methods: Blood mononuclear cells from healthy volunteers (n=10, Normal) and septic shock patients (n=10, SS) were isolated and cultured. Culture plate adherent monocytes were incubated with either medium (Control) or LPS (LPS) for 18 hours at 31°C. The supernatant was collected and analyzed for TNF-α and IL-10 by ELISA. Values are mean ± SEM, * p,0.05 vs. control Results TNF- α ng/ml Normal SS Control .54±.12 .82±.25 LPS 3.26±1* 1.26±.31 IL-10 pg/ml ...
TY - JOUR. T1 - Monoclonal anti-tumor necrosis factor antibody renders non-obese diabetic mice hypersensitive to irradiation and enhances insulitis development. AU - Jacob, Chalm O.. AU - Aiso, Sadakazu. AU - Schreiber, Robert D.. AU - Mcdevitt, Hugh O.. PY - 1992/5/1. Y1 - 1992/5/1. N2 - In attempt to evaluate biological roles of tumor necrosis factor (TNF), we studied the effects of anti-TNF mAb in non-obese diabetic (NOD) mice. Anti-murine TNF mAb rendered NOD mice hypersensitive to the lethal effects of radiation and prevented the reconstitution of lethally Irradiated mice with adoptively transferred lymphocytes. While TNF-α reduced the incidence of diabetes development in the adoptive transfer system even when given 6 days post-transfer, mAb to TNF could not reduce or increase the incidence of diabetes compared to control mice. Administration of TNF-α for 4 or 8 weeks significantly reduced the Incidence of spontaneous Insulitis in NOD mice, while antl-TNF mAb given for 8 weeks Increased ...
Crystals of tumor necrosis factor (TNF) have been obtained in two forms. Rhombohedral crystals grow in 1.8 to 2.0 M ammonium sulfite, pH 7.8 at 21 degrees C, and tetragonal crystals grow in 2.6 M magnesium sulfate, pH 5.5 at 25 degrees C. Analysis of TNF by isoelectric focusing under native and denaturing conditions indicates that TNF molecules exist as trimers in solution. The rhombohedral cachectin crystals belong to space group R3 and have unit cell constants a = b = c = 47.65 A and alpha = beta = gamma = 88.1 degrees. Density determinations and the space group indicate that the unit cell contains one 51,000-dalton trimer. These crystals are stable in the x-ray beam and diffract to at least 1.85 A but are apparently twinned by merohedry. The tetragonal crystals are space group P4(3)2(1)2 or its enantiomorph P4(1)2(1)2 and have unit cell constants a = b = 95.08, c = 117.49. The asymmetric unit contains one trimer; the crystals are stable in the x-ray beam and diffract to beyond 3 A ...
OBJECTIVE: To evaluate the efficacy, pharmacokinetics, immunogenicity, and safety of multiple infusions of a chimeric monoclonal anti-tumor necrosis factor alpha antibody (cA2) (infliximab; Remicade, Centocor, Malvern, PA) given alone or in combination with low-dose methotrexate (MTX) in rheumatoid arthritis (RA) patients. METHODS: In a 26-week, double-blind, placebo-controlled, multicenter trial, 101 patients with active RA exhibiting an incomplete response or flare of disease activity while receiving low-dose MTX were randomized to 1 of 7 groups of 14-15 patients each. The patients received either intravenous cA2 at 1, 3, or 10 mg/kg, with or without MTX 7.5 mg/week, or intravenous placebo plus MTX 7.5 mg/week at weeks 0, 2, 6, 10, and 14 and were followed up through week 26. RESULTS: Approximately 60% of patients receiving cA2 at 3 or 10 mg/kg with or without MTX achieved the 20% Paulus criteria for response to treatment, for a median duration of 10.4 to |18.1 weeks (P | 0.001 versus placebo).
1. Bertone-Johnson ER. Chronic inflammation and premenstrual syndrome: a missing link found? J Womens Health (Larchmt). 2016 Sep;25(9):857-8. doi: 10.1089/jwh.2016.5937.. 2. Ezaki K, Motoyama H, Sasaki H. Immunohistologic localization of estrone sulfatase in uterine endometrium and adenomyosis. Obstet Gynecol. 2001 Nov;98(5 Pt 1):815-9.. 3. Gao L, Gu Y, Yin X. High serum tumor necrosis factor-alpha levels in women with polycystic ovary syndrome: a meta-analysis. PLoS One. 2016 Oct 20;11(10):e0164021. doi: 10.1371/journal.pone.0164021.. 4. Alpañés M, Fernández-Durán E, Escobar-Morreale HF. Androgens and polycystic ovary syndrome. Expert Rev Endocrinol Metab. 2012;7(1):91-102.. 5. Niswender GD, Juengel JL, Silva PJ, Rollyson MK, McIntush EW. Mechanisms controlling the function and life span of the corpus luteum. Physiol Rev. 2000 Jan;80(1):1-29.. 6. Gore AC, Chappell VA, Fenton SE, Flaws JA, Nadal A, Prins GS, et al. Executive Summary to EDC-2: The Endocrine Societys Second Scientific ...
Aged,Antibodies, Monoclonal/adverse effects,Antibodies, Monoclonal, Humanized,Antirheumatic Agents/*adverse effects,Arthritis, Rheumatoid/*drug therapy,Drug Eruptions/*etiology/pathology,Female,Granuloma Annulare/*chemically induced/pathology,Humans,Immunoglobulin G/adverse effects,Male,Middle Aged,Receptors, Tumor Necrosis Factor,Tumor Necrosis Factor-alpha/*antagonists & ...
This new market research report forecasts on Tumor Necrosis Factor Market providing complete market figures, consisting market size and estimation by Tumor Necrosis Factor Market application and products depending upon geographical location for the forecasting period 2017 to 2025. Further, the Tumor Necrosis Factor Market research report study also encompasses complete industry background, with Tumor Necrosis Factor Market drivers, competitive market dynamics, market restraints, market growth opportunities, industry challenges and critical success factors (CSFs). The Tumor Necrosis Factor Market research report examines top industry competitors, offering organization market share analysis and detailed outlines of these firms, with product benchmarking.. Browse Full Report Visit - http://bit.ly/2iHZppr. Reasons to Buy This Report :. ...
Eosinophils play a central role in asthma. The present study was performed to investigate the effect of tumour necrosis factor-α (TNF-α) on longevity of isolated human eosinophils. In contrast to Fas, TNF-α inhibited eosinophil apoptosis as evidenced by a combination of flow cytometry, DNA fragmentation assay and morphological analyses. The effect of TNF-α on eosinophil apoptosis was reversed by a TNF-α neutralising antibody. The anti-apoptotic effect of TNF-α was not due to autocrine release of known survival-prolonging cytokines interleukins 3 and 5 or granulocyte-macrophage-colony-stimulatin​gfactor as their neutralisation did not affect the effect of TNF-α. The anti-apoptotic signal was mediated mainly by the TNF-receptor 1. TNF-α induced phosphorylation and degradation of IκB and an increase in NF-κB DNA-binding activity. The survival-prolonging effect of TNF-α was reversed by inhibitors of NF-κB pyrrolidinedithiocarbamate and gliotoxin and by an inhibitor of IκB kinase, ...
TY - JOUR. T1 - Tumor necrosis factor inhibitors in patients with Takayasu arteritis. T2 - Experience from a referral center with long-term followup. AU - Schmidt, Jean. AU - Kermani, Tanaz A.. AU - Bacani, A. Kirstin. AU - Crowson, Cynthia S.. AU - Matteson, Eric L.. AU - Warrington, Kenneth J.. PY - 2012/7/1. Y1 - 2012/7/1. N2 - Objective. To report a single-center experience with the use of tumor necrosis factor (TNF) inhibitors in patients with Takayasu arteritis (TA). Methods. We retrospectively studied a cohort of patients with refractory TA evaluated at our institution and treated with TNF inhibitors. American College of Rheumatology criteria for TA were used for inclusion. Disease activity was assessed according to the National Institutes of Health criteria. Results. We included 20 patients (19 women, 17 white) with a mean ± SD age of 33 ± 10.2 years and a median disease duration of 15.9 months (interquartile range [IRQ] 2-32.7 months) prior to the use of TNF inhibitors. Before the use ...
The rationale for anti-tumour necrosis factor-alpha (anti-TNFalpha) therapy in rheumatoid arthritis (RA) is based on experiments on cultures of human rheumatoidjoint tissue, supported by experiments in animal models, all of which demonstrated that anti-TNFalpha antibody had profound effects on the
C3a and C5a anaphylatoxins are two proinflammatory peptides generated during complement activation that act through distinct G$_i$ protein-coupled receptors named C3aR and C5aR, respectively. We have demonstrated previously that human astrocytes expressed C3aR and C5aR constitutively and were able to produce a functional complement. In this study, we examined the effect of an anaphylatoxin stimulation on cytokine expression by human astrocyte cell lines. Interleukin (IL)-1$\beta$, IL-6, tumor necrosis factor-\alpha$, and transforming growth factor-$\beta$ mRNA expression was studied by quantitative RT-PCR. Whereas IL-1$\beta$, tumor necrosis factor-$\alpha$, and transforming growth factor-$\beta$ mRNA levels remained unchanged, stimulation of astrocytoma cells (T98G, CB193, U118MG) by C3a, C5a, and peptidic C3aR and C5aR agonists induced an increase in the IL-6 mRNA level. The amount of IL-6 was markedly increased at 3 and 6 h and returned to the basal level at 9 h of stimulation. This response was
Effects of interferons and tumour necrosis factor-a on human lung cancer cell lines and the development of an interferon-resistant lung cancer cell line. ...
With the success of the human genome project, the focus of life science research has shifted to the functional and structural analyses of proteins, such as the fields of proteomics and structural genomics. These analyses of proteins, including newly identified proteins, are expected to contribute to the identification of therapeutically applicable proteins for various diseases. Thus, pharmacoproteomic-based drug discovery and the development of protein therapies has currently attracted a great deal of attention (1, 2, 3) . However, it is clinically difficult to use most bioactive proteins, such as tumor necrosis factor-α (TNF-α), as antitumor agents because of their very low stability and pleiotropic action in vivo (4 , 5) .. TNF-α was reported to exert a strong cytotoxicity to various kinds of tumor cells but not to normal cells in vitro and to cause hemorrhagic necrosis of certain transplanted solid tumors (6) . Thus, TNF-α has been considered a promising new drug for cancer therapy. On ...
The anti-inflammatory/antiallergic activity of a novel second-generation p38 mitogen-activated protein kinase inhibitor, SB 239063 [trans-1-(4-hydroxycyclohexyl)-4-(4-fluorophenyl)-5-(2-methoxypyridimidin-4-yl)imidazole], was investigated in vivo and in vitro. SB 239063 had an IC50 of 44 nM for inhibition of recombinant purified human p38α. In lipopolysaccharide-stimulated human peripheral blood monocytes, SB 239063 inhibited interleukin-1 and tumor necrosis factor-α production (IC50 values = 0.12 and 0.35 μM, respectively). A role for p38 kinase in cytokine-associated inflammation in the mouse was shown by p38 activation in the lung and inhibition of lipopolysaccharide-induced tumor necrosis factor-α production by SB 239063 (ED50 = 5.8 mg/kg p.o.). Antiallergic activity was demonstrated by essential abolition (∼93% inhibition) of inhaled ovalbumin (OA)-induced airway eosinophilia by SB 239063 (12 mg/kg p.o.), measured by bronchoalveolar lavage (BAL) in OA-sensitized mice. In addition, p38 ...
Listeriosis in mice with the severe combined immunodeficiency (SCID) mutation is an established model in vivo and in vitro of interferon gamma (IFN-gamma)-dependent macrophage activation by natural killer (NK) cells during the development of natural immunity. We demonstrate that IFN-gamma production from SCID splenocytes is stimulated by interleukin (IL) 12, tumor necrosis factor alpha (TNF-alpha), and IL-2 but is inhibited by IL-10, IL-10, IL-12, and TNF are induced by heat-killed Listeria monocytogenes (hk-LM) from SCID splenocytes and peritoneal macrophages. IL-12 production is necessary for hk-LM to stimulate IFN-gamma production by SCID splenocytes since neutralization of IL-12 totally blocks IFN-gamma production in this system. TNF-alpha and IL-2 act synergistically with IL-12 to augment IFN-gamma production. Also, exogenous IL-2 increases the response of NK cells to hk-LM or to IL-12 and TNF-alpha. In contrast, IL-10 inhibits hk-LM-induced IFN-gamma production at two levels: (i) by ...
Results: Atorvastatin significantly decreased liver transaminase, gamma-glutamyl transpeptidase, low-density lipoprotein-cholesterol, triglycerides, type IV collagen, and tumour necrosis factor-alpha levels, whilst it increased adiponectin and high-density lipoprotein-cholesterol. Atorvastatin improved nonalcoholic fatty liver disease activity score and increased liver to spleen density ratio. Multiple stepwise regression analysis revealed that gamma-glutamyl transpeptidase, tumour necrosis factor-alpha and liver to spleen density ratio ( inversely) were independently associated with nonalcoholic fatty liver disease activity score. Aspartate aminotransferase, low-density lipoprotein-cholesterol and nonalcoholic fatty liver disease activity score were independent determinants of decreased liver to spleen density ratio ...
Roh M, Zhang Y, Murakami Y, Thanos A, Lee SC, Vavvas DG, Benowitz LI, Miller JW. Etanercept, a widely used inhibitor of tumor necrosis factor-α (TNF-α), prevents retinal ganglion cell loss in a rat model of glaucoma. PLoS One 2012;7(7):e40065.
Severe infection and sepsis are common causes of morbidity and mortality. Early diagnosis in critically ill patients is important to reduce these complications. The present study was conducted to determine the role of serum leptin at early diagnosis and differentiation between patients with manifestations of systemic inflammatory response syndrome (SIRS) and those with sepsis in patients suffering from a broad range of diseases in the intensive care unit (ICU) and its correlation with other biomarkers, such as C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). One hundred and six adult ICU patients were observed. CRP, leptin, IL-6 and TNF-α were compared among the following groups: sepsis group (n = 40), SIRS group (n = 34) and non-SIRS group (n = 32). Patients were classified into these groups at the time of blood analysis for these biomarkers. Non-significant differences were observed among patients in different groups regarding biomarkers on the day of ICU
Vascular calcification is implicated in many diseases including atherosclerosis and diabetes. Tumor necrosis factor-α (TNF-α) has been shown to promote vascular calcification both in vitro and in vivo. However, the molecular mechanism of TNF-α-mediated vascular calcification has not yet been fully defined. Therefore, in this study, we aimed to investigate whether MSX2 acts as a crucial regulator in TNF-α-induced vascular calcification and to define the regulatory mechanism of MSX2 induction in human vascular smooth muscle cells (VSMCs ...
RPB499Hu01, CD120A; P55; TBP1; FPF; TNF-R; TNF-R-I; TNF-R55; TNFAR; TNFR1; TNFR55; TNFR60; P55-R; P60; Tumor necrosis factor receptor 1; Tumor necrosis factor-binding protein 1 | Products for research use only!
TY - JOUR. T1 - Role of tumor necrosis factor in preovulatory follicles of swine. AU - Prange-Kiel, J.. AU - Kreutzkamm, C.. AU - Wehrenberg, U.. AU - Rune, G. M.. PY - 2001. Y1 - 2001. N2 - The effects of tumor necrosis factor (TNF) on cultured porcine granulosa cells that were obtained from preovulatory follicles were studied with regard to following parameters: 1) TNF receptor type I expression, 2) progesterone receptor and transforming growth factor β receptor type II (TβR II) as markers of luteinization, 3) proliferation, and 4) apoptosis. For comparative purposes the effects of TNF were also studied on insulin/forskolin-treated cells, as this treatment is well established to induce luteinization. Cytochemical methods followed by semiquantitative analysis were used. Our data show that TNF treatment upregulates TNF receptor type I expression in granulosa cells. TNF downregulates the expression of TβR II of insulin/forskolin-stimulated and of unstimulated cells. The progesterone receptor ...
Tumour necrosis factor production by monocytes from cattle infected with Trypanosoma (Duttonella) vivax and Trypanosoma (Nannomonas) congolense STI possible association with severity of anaemia associated with the ...
1. The effects of recombinant human tumour necrosis factor alpha (TNF) and murine interleukin-1 alpha (IL-1) on the activation state of the hepatic pyruvate dehydrogenase complex (PDHa), the activity of mitochondrial PDH kinase, hepatic lipogenesis de novo and plasma triacylglycerol (TG) concentrations were studied. 2. Monokine effects depended upon prior nutritional state. In rats fasted for 20 h or 45 h before monokine administration and refeeding (orally or with intravenous glucose), PDHa, TG and hepatic lipogenesis were not increased. In rats fed ad libitum, treatment with TNF plus IL-1 increased the contribution of hepatic lipogenesis to circulating TG to 550% of control values (P = 0.03) and plasma TG concentrations to 159% (P = 0.02), whereas PDHa increased slightly to 120% (P = 0.02) and liver glycogen content fell to 45.8% (P = 0.05) of control values. 3. Intrinsic hepatic PDH kinase activity was not changed by monokine treatment in rats fed ad libitum. 4. The increased lipogenesis de ...
TY - JOUR. T1 - Anti-tumor necrosis factor-a treatment with infliximab for disseminated granuloma annulare. AU - Murdaca, Giuseppe. AU - Colombo, Barbara Maria. AU - Barabino, Gianfranco. AU - Caiti, Matteo. AU - Cagnati, Paola. AU - Puppo, Francesco. PY - 2010. Y1 - 2010. N2 - Granuloma annulare (GA) is a chronic inflammatory disease of unknown etiology characterized by the development of plaques preferentially localized to the distal extremities. Spontaneous remission and relapses are quite common and the course of GA is not easy to predict. Moreover, most therapeutic regimens have been used anecdotally and with variable success. We report the case of a 62-year-old White female patient affected by disseminated GA unsuccessfully treated with psoralen plus UVA photochemotherapy, prednisone, and cyclosporine (ciclosporin) who responded to the anti-tumor necrosis factor-a monoclonal antibody infliximab administered intravenously at a dosage of 5mg/kg at weeks 0, 2, and 6 and thereafter at monthly ...
TY - JOUR. T1 - Erythropoietin fails to reverse the anemia in mice continuously exposed to tumor necrosis factor-alpha in vivo. AU - Clibon, U.. AU - Bonewald, Lynda. AU - Caro, J.. AU - Roodman, G. David. PY - 1990. Y1 - 1990. N2 - Tumor necrosis factor-α (TNF) is a monokine produced by activated macrophages that has cytotoxic and cytostatic effects on erythroid progenitor cells. We have recently shown that Chinese hamster ovary cells transfected with the human TNF gene and which constitutively express TNF induced a hypoproliferative anemia, mild thrombocytopenia, and mild leukocytosis when injected into nude mice. We have used this murine model to determine if treatment with recombinant human erythropoietin can prevent or ameliorate the anemia seen with long-term continuous exposure to high concentrations of TNF. Mice bearing TNF-producing tumors became anemic with hematocrits ranging from 30 to 32%. Treatment with recombinant human erythropoietin (100-1000 U/kg body weight three times per ...
The genomic sequencing technique has been applied to assess the state of methylation in the DNA from human leukocyte subpopulations from healthy individuals and in the DNA from several individuals with myeloid or lymphatic leukemias or non-Hodgkin lymphomas. Leukocyte populations were purified by the high-gradient magnetic cell sorting technique. In the human tumor necrosis factor alpha (TNF-alpha) gene segment between nucleotides 300 and 1150, the specific methylation profile in the DNA from human granulocytes and monocytes is maintained in three cases of myeloid leukemia. In one such case, all 5-methyl-2-deoxycytidine residues have been replaced by cytidine. In a chronic lymphatic T-cell leukemia, all 5-methyl-2-deoxycytidine residues have been substituted by cytidine. In normal B lymphocytes, in two cases of chronic lymphatic B-cell leukemias and two cases of non-Hodgkin lymphomas, all 5-CG-3 sequences in this gene segment are devoid of methylation. In the TNF-beta gene, DNA methylation is
Tnfrsf1a (untagged) - Mouse tumor necrosis factor receptor superfamily, member 1a (cDNA clone MGC:6117 IMAGE:3585060), (10ug), 10 µg.
Patients with chronic low back pain (cLBP) have high rates of comorbid psychiatric disorders, mainly depression. Recent evidence suggests that depressive symptoms and pain, as interacting factors, have an effect on the circulating levels of inflammatory markers relevant to coronary artery disease. Our previous work showed a higher serum level of an inflammatory marker tumour necrosis factor-alpha (TNFα) in patients with cLBP, which did not correlate with intensity of low back pain alone. In the present study we investigated the cross-sectional associations of depressive symptoms, low back pain and their interaction with circulating levels of TNFα. Each group of 29 patients with cLBP alone or with both cLBP and depression was age-matched and sex-matched with 29 healthy controls. All subjects underwent a blood draw for the assessment of serum TNFα and completed a standardised questionnaire regarding medication, depression scores according to the German version of Centre for Epidemiological Studies