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Dissertations / Theses on the topic 'Tumor necrosis factor alpha (TNFalpha)'

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Published: 11 March 2023

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1

Dinnetz, Joyce Marie. "Omega-3 fatty acid supplementation reduces basal TNFalpha but not toll-like receptor stimulated TNFalpha in full sized and miniature mares." Thesis, Manhattan, Kan. : Kansas State University, 2009. http://hdl.handle.net/2097/1497.

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2

Beck, Eichler-Jonsson Claudia. "Aspects of mitogen-activated protein kinase cascade activation by epidermal growth factor (EGF): kinetics and crosstalk mechanism with tumor necrosis factor Alpha (TNFalpha) /." [S.l. : s.n.], 2002. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10252924.

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3

Derouich-Guergour, Dorra. "Etude de la régulation de l'expression des récepteurs du Tumor Necrosis Factor alpha (TNFalpha) au cours de l'infection par Toxoplasma gondii (modèle humain in vitro)." Université Joseph Fourier (Grenoble), 2001. http://www.theses.fr/2001GRE10162.

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Toxoplasma gondii est un protozoaire opportuniste responsable de la toxoplasmose, affection pouvant entraîner des atteintes cliniques graves chez les immunodéprimés et en cas d'atteintes congénitales. Le TNF[alpha], cytokine pro-inflammatoire, a une importance primordiale dans le contrôle de l'infection toxoplasmique. Elle agit par l'intermédiaire de deux récepteurs membranaires :TNFR1 et TNFR2. Nous avons étudié l'expression des récepteurs du TNF[alpha] au cours de l'infection de cellules humaines fibroblastiques MRC5 et de cellules myélomonocutaires THP-1 par T. Gondii. La modulation des TNFRs PAR T. Gondii, in vitro, semble dépendre du type cellulaire utilisé. Nos résultats indiquent que l'infection de cellules d'origine macrophagique (THP-1) par les tachyzoi͏̈tes de la souche RH de T. Gondii est responsable d'une baisse des TNFRs membranaires associée à une augmentation de la libération de TNFR1 solubles dans le milieu de culture. Nous montrons également qu'une pénétration active des parasites est nécessaire et que certains antigènes parasitaires thermosensibles semblent être impliqués. Ce mécanisme de régulation des TNFRs pourrait influencer le rôle du TNF[alpha] dans la toxoplasmose. En effet, ces formes solubles produites par clivage protéolytique des récepteurs membranaires sont capables de se fixer au TNF[alpha] et de réguler sa bio-activité.

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4

Molgat, André. "The Effect of Macrophage-secreted Factors on Preadipocyte Survival." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23628.

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Adipose tissue (AT) expansion and remodeling that maintains healthy function relies on stromal preadipocytes capable of differentiating into new adipocytes (adipogenesis). During chronic positive energy balance, a relative deficit in adipogenesis, from either a decrease in preadipocyte number or their capacity to differentiate, leads to excessive adipocyte hypertrophy and AT dysfunction. AT contains macrophages whose number and activation state is dynamically regulated with changes in AT mass. This study aims to investigate the effect of macrophage-secreted factors on preadipocyte survival. To assess the effect of macrophage-secreted factors on preadipocytes, murine 3T3-L1 preadipocytes or human primary preadipocytes were incubated with macrophage-conditioned medium (MacCM), prepared from either murine (J774A.1, RAW264.7, bone marrow-derived) or human (THP-1, monocyte-derived) macrophage models, respectively. MacCM inhibited preadipocyte apoptosis and activated pro-survival signaling in both preadipocyte models. Inhibition of PDGFR, Akt, or ERK1/2 reduced the pro-survival effect of MacCM in 3T3-L1 preadipocytes. Inhibition of reactive oxygen species (ROS) generation, or enhancement of ROS clearance, reduced MacCM-dependent 3T3-L1 preadipocyte survival. Whereas anti-inflammatory activated macrophages retained the ability to prevent preadipocyte apoptosis, pro-inflammatory activated macrophages did not. TNF-α immunoneutralization restored the survival activity of pro-inflammatory MacCM on 3T3-L1 preadipocytes. These studies reveal a novel pro-survival effect of MacCM on preadipocytes, and identify signaling molecules (PDGF, Akt, ERK1/2, and ROS) that underlie this action. Macrophage activation was found to regulate the pro-survival activity of MacCM. These in vitro cell culture studies are consistent with a model in which the extent of preadipocyte apoptosis in vivo may determine preadipocyte number and the ability of AT to expand while maintaining healthy function during chronic positive energy balance.

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5

Atkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha /." Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha878.pdf.

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6

Watts, Alan D. "The biological role of transmembrane tumour necrosis factor [alpha]." Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27668.

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Tumour necrosis factor (TNF) exists in two physiological forms. One is a soluble polypeptide of 17 kDa, and the other a type II integral membrane protein of 26 kDa designated transmembrane TNF. Soluble TNF is derived from the transmembrane form by proteolytic processing. The soluble TNF molecule exerts potent cytotoxic activity against certain types of cancer cells, and plays a critical role in the functioning of the immune and inflammatory system. The transmembrane TNF molecule shares many of the properties of the soluble form in vitro, but its function in the immune system is not as clearly defined as for the sTNF form. In this thesis the biological role of transmembrane TNF was investigated. The synthesis and expression of both soluble TNF and transmembrane TNF forms was examined in macrophage cells stimulated with LPS. Basic parameters for the production of transmembrane TNF were established to enable further analysis of its function. Using a hydroxamic acid-based inhibitor of TNF processing it was possible to obtain macrophage cells that expressed transmembrane TNF, but not soluble TNF; This enabled the investigation of transmembrane TNF free from the complicating effects of soluble TNF. It was found that inhibition of TNF processing in this way caused an accumulation of transmembrane TNF on the macrophage cells surface 5.1-7.5-fold greater than in cells not treated with the hydroxamic acid-based inhibitor. This corresponded to a 6.4-fold increase in TNF-mediated cytotoxicity of macrophage cells towards cells sensitive to transmembrane TNF. By radiolabelling macrophages, and using a specialised immunoprecipitation method, it was demonstrated that a soluble form of one of the TNF receptors (sTNFFi) binds transmembrane TNF. The consequence of this binding was neutralisation of transmembrane TNF-mediated cytotoxicity, but not inhibition of proteolytic processing of transmembrane TNF to release soluble TNF. The possibility that transmembrane TNF is capable of transducing a signal upon ligation with sTNFR was investigated. A broad range of cellular parameters were measured to see whether sTNFFi treatment of macrophages expressing transmembrane TNF induced a biochemical/physiochemical change. It was found that sTNFR caused a large increase (~200%) in ix intracellular calcium levels after 15 min treatment. This is the first direct evidence that transmembrane TNF is capable of acting like a receptor. The composition of the predicted amino acid sequence of transmembrane TNF was closely examined to determine the presence of features important for both structure and intracellular signalling. A model is presented in Chapter 6 which outlines in diagrammatic form likely structural features of transmembrane TNF. The molecule is predicted to possess a region of cytoplasmic alpha-helices corresponding to a highly conserved domain of the sequence. The structure of transmembrane TNF is consistent with that of a transmembrane receptor, capable of transducing signals initiated by ligation with an extracellular ligand. The comparison of predicted amino acid sequences of transmembrane TNF from different mammalian species revealed the presence of a conserved casein kinase | site. This site was also found to be present in most members of the TNF ligand family. Using orthophosphate labelling, it was shown that mouse transmembrane TNF is phosphorylated in macrophages. Ligation of sTNFR with transmembrane TNF induced de-phosphorylation of mTNF. This de-phosphorylation could be prevented by pre-incubation of the cells with serine phosphatase inhibitors. A selective inhibitor of casein kinase | dramatically reduced the phosphorylation of transmembrane TNF produced by macrophages. In addition, a recombinant form of casein kinase l phosphorylated transmembrane TNF in vitro on the site naturally phosphorylated by the endogenous kinase in vivo. The evidence presented in this study supports an entirely new role for transmembrane TNF, one in which the molecule is capable of acting like a transmembrane receptor, with the ligand being sTNFR. This phenomenon is known as "reverse signalling", and has been shown by other researchers to occur in the majority of members of the TNF ligand family. Implications of mTNF "reverse signalling" are relevant to the treatment of human diseases in which sTNFRs are currently being assessed in clinical trials.

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7

Nguyen, Thanh Minh. "Tumor necrosis factor alpha (TNF-[alpha]) signal transduction pathways in cyclooxygenase-2 expression /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486459267519688.

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8

Babu, Kesavan Suresh. "The role of tumor necrosis factor alpha (TNF-Î±) in asthma." Thesis, University of Southampton, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439378.

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9

Bond, Arden Lenore. "The production and characterization of a putative anti-idiotypic antibody to tumor necrosis factor-[alpha] /." This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-05042010-020132/.

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10

Hurst, Liam Andrew. "The role of tumour necrosis factor alpha in pulmonary arterial hypertension." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648471.

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11

Yang, Junbao. "Genetic engineering of a fusion protein possessing anti-tumor Fv and tumor necrosis factor alpha." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0030/NQ63940.pdf.

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12

Zwaveling, Jan Harm. "Systemic side effects of isolated limb perfusion with tumor necrosis factor alpha." [S.l. : [Groningen] : s.n.] ; [University Library Groningen] [Host], 1997. http://irs.ub.rug.nl/ppn/15723665X.

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13

Hakim, Akhlaq Waheed. "Tumor necrosis factor alpha and non-inflammatory sensitization of masseter muscle nociceptors." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/34182.

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Behavioral evidence in rats indicates that injection of tumor necrosis factor alpha (TNFalpha into skeletal muscle results in a prolonged mechanical sensitization without gross inflammation. The present series of studies were conducted to test the idea that injection of TNFalpha causes mechanical sensitization of skeletal muscle through a peripheral mechanism that involves lowering of the mechanical threshold (MT) of muscle nociceptors without inflammation. In- vivo extracellular electrophysiological recording was used to assess the effect of TNFalpha (1 or 0.1microgram) and other drugs on the excitability and MT of masseter muscle nociceptors. Expression of TNFR1 (P55) and TNFR2 (P75) receptors by the masseter muscle and trigeminal ganglion neurons that innervate that muscle was determined by Western blot and immunohistochemical methodologies, respectively. The Evans blue dye technique and thermal camera recordings were used to assess inflammation in muscle tissues. Enzyme-linked immunoassays and glutamate biosensor probes were used to measure muscle concentrations of prostaglandin (PG) E2 and nerve growth factor, and glutamate, respectively. Intramuscular injection of 1mg TNFalpha did not excite nociceptors, but did significantly decrease MT compared to vehicle control. There was no evidence of gross inflammation 3 hours after injection of TNFalpha. Co-injection of TNFalpha with P55 or P75 receptor antibodies attenuated TNFalpha-induced mechanical sensitization. P55 and P75 receptors were expressed by 29% and 62% of masseter nociceptors, respectively. PGE2 and glutamate concentrations were significantly changed 3 hours after TNFalpha injection into the masseter muscle. Injection of diclofenac, a cycloxygenase inhibitor that attenuates prostaglandin synthesis, partially reversed the TNFalpha-induced decreases in the MT of masseter muscle nociceptors, while vehicle control, DL-2-amino-5-phophonovaleric acid, a competitive NMDA receptor antagonist, and a tyrosine kinase A receptor antibody, which blocks NGF-induced masseter muscle nociceptor sensitization, did not significantly alter nociceptor MT. These findings indicate that TNFalpha-induced mechanical sensitization of masseter nociceptors is mediated, in part, by increased PGE2 levels through activation of peripheral P55 and P75 receptors. Over all, these results suggest that injection of TNFalpha into skeletal muscle could be used as a model of myofascial trigger points to study the peripheral pain mechanisms of masticatory muscle pain.

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14

Mallet, Dominique. "Interet du tumor necrosis factor alpha dans le suivi precoce des transplantations renales." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20913.

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15

Atzeni, Fabiola. "Antibody profiles in patients treated with tumor necrosis factor-alpha antagonists: new findings." Doctoral thesis, Universitat Autònoma de Barcelona, 2005. http://hdl.handle.net/10803/3771.

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It has been reported that patients with rheumatoid arthritis (RA), Crohn's disease (CD) and spondyloarthritis (SpA) treated with selective tumor necrosis factor-alpha (TNF-?) inhibitors develop autoantibodies such as antinuclear antibodies (ANA) and anti-double stranded DNA (anti-dsDNA) antibodies. TNF-? is a pro-inflammatory cytokine that is produced by multiple cell types, including blood monocytes, macrophages, mast cells and endothelial cells, and plays multiple complex functional roles within the immune system, including the stimulation of inflammation, cytotoxicity, the regulation cell adhesion and the induction of cachexia. There are therefore a number of potential mechanisms by means of which anti-TNF-? treatment could be beneficial in RA, CD and other diseases. RA is a chronic inflammatory disease that primarily affects the peripheral joints and often leads to tissue degradation and the destruction of bone and cartilage. As organic joint damage is irreversible, it is important to recognise and treat RA early with the aim of halting its progression. Clinical trials have demonstrated that TNF-? blocking agents are highly beneficial for most patients with RA refractory to classic treatment with disease-modifying antirheumatic drugs (DMARDs), but a significant number also fail to respond to anti-TNF-? therapy. No reliable predictive markers of a clinical response have been identified, although a recent report suggests that reduced rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibody levels may be useful adjuncts when assessing treatment efficacy.
A reduction in IgM-RF titres was initially described by Charles et al. in a small series of patients receiving infliximab, but the subsequent findings were inconsistent. Two recent studies have found decreased RF and anti-CCP antibody titres in RA patients treated with infliximab. In both cases, decrease paralleled the improvements in the disease activity scores, but one group reported a return to baseline levels when the follow-up was extended to 54 and 78 weeks. However, De Rycke et al. showed that RF, but not anti-CCP antibodies, is modulated by infliximab in RA and our findings support the existing evidence that RF and anti-CCP antibodies are independent autoantibody systems in RA. CD is a chronic inflammatory disease of the gastrointestinal tract whose variable clinical course is characterised by segmental transmural inflammation and granulomatous changes of unknown origin. Infliximab is a chimeric IgG1 monoclonal anti-TNF-? antibody that represents a significant advance in the treatment of CD. Controlled clinical trials have demonstrated its effectiveness in rapidly induces and maintains remission in patients with moderate/severe refractory CD, healing endoscopic lesions, and treating draining perianal (PA) fistulae in the short and long term. Moreover, audit data from North America and Europe have shown that its efficacy in clinical practice is comparable with that observed in clinical trials. Trials have shown that CD and RA patients develop ANAs and anti-dsDNA antibodies: according to the reported safety data, respectively 63.8% and 49.1% of patients develop newly positive ANAs during infliximab treatment, and respectively 13% and 21.5% develop newly positive anti-dsDNA antibodies. Two important papers have described the risk of immunogenicity induced by infliximab treatment in CD patients: Baert et al. showed that the development of antibodies against infliximab leads to infusion reactions and a shorter treatment response to treatment and, as concomitant immunosuppressive therapy reduces the magnitude of the immunogenic response, concluded that it is necessary to combine methotrexate (MTX) and infliximab in order to reduce the risk of the appearance of anti-idiotypic autoantibodies; and Vermeire et al. found a cumulative 24-month incidence of ANAs in 71/125 patients (56.8%), almost half of whom developed ANAs after the first infusion and >75% became ANApositive after fewer than three infusions. However, lower percentages have been reported in patients treated with etanercept. Interestingly, these autoantibodies have been only anecdotally associated with clinical manifestations suggesting drug-induced systemic lupus erythematosus (SLE). It was thought that the absence of such an association was related to the IgM or IgA isotypes of anti-dsDNA antibodies, as well as low antibody affinity (in contrast with the widely accepted relationship between SLE and the high affinity IgG isotype). However, the occurrence of these autoantibodies is now considered a drug class-related side effect, despite the higher prevalence of ANAs and anti-dsDNA antibodies in patients treated with infliximab than in those treated with etanercept, and the absence of a flare when etanercept therapy was started in a patient with previous infliximab-induced SLE. Finally, anti-phospholipid antibodies (aPL), which are mainly detectable by means of anti-cardiolipin assay (aCL), have also been reported in RA patients receiving TNF-? blockers. In some cases, their appearance was related to concomitant infectious processes, but no clear correlation was found with the specific clinical manifestations of anti-phospholipid syndrome, although one paper suggests that they may predict a poor clinical outcome.
The aim of this thesis is to evaluate prospectively the auto-antibody profiles of CD and RA patients treated with infliximab and adalimumab, and their relationships to clinical outcomes.
In particular, the aim of the first one-year prospective study was planned to evaluated: a) the clinical efficacy of adalimumab; b) whether the prevalence and titres of RAassociated auto-antibodies, such as RF and anti-CCP antibodies correlate with treatment effect; and c) whether non organ-specific auto-antibodies are induced by adalimumab like other TNF-? blocking agents.
The aim of the second study was evaluated: the frequency and correlation of autoantibody development at standardised timepoints in refractory/inflammatory and fistulising CD patients in a routine clinical setting. Finally, the findings were related to disease status before the start of infliximab treatment, the response to infliximab treatment and the onset of adverse clinical events.
The first part of this thesis considers the role of TNF-? in RA and CD, and the efficacy of anti-TNF-? agents in inducing auto-antibodies (including two recent reviews by our group and a recently published case report); the second evaluates the mechanisms involved in auto-antibody development in CD and RA patients receiving anti-TNF-? treatment; and the third briefly summarises two original studies, together with their discussion and conclusions.

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16

Rogers, Gabrielle Marie. "Tumor necrosis factor- alpha production induced by peptidoglycan-polysaccharide in early pregnant ewes." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4712.

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Thesis (M.S.)--West Virginia University, 2006.
Title from document title page. Document formatted into pages; contains vi, 45 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 40-45).

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17

Fisher, Anat. "Comparative persistence of tumor necrosis factor alpha antagonists in patients with rheumatoid arthritis." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43055.

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Introduction: This thesis comprises three studies examining treatment persistence with tumour necrosis factor alpha (TNFα) antagonists in rheumatoid arthritis (RA) patients. Persistence, also commonly known as duration of treatment, has been suggested as an indirect measure that balances benefit and harm, and it is important for cost-effectiveness analysis and budget planning. Previous research has examined the effect of drug and patient characteristics on persistence with TNFα antagonists. Objectives: 1) To estimate pairwise comparative persistence with TNFα antagonists infliximab, adalimumab and etanercept in RA patients; 2) To evaluate the impact of investigator factors (methods) and of prescriber factors (propensity for discontinuation and preference for prescribed drug) on comparative persistence estimates with TNFα antagonists in RA patients . Methods: To address these objectives, three population-based studies of an RA cohort were conducted in British Columbia patients using survival analysis methodology. Results: 1) In RA patients similar persistence was observed with infliximab, adalimumab and etanercept, with median persistence equaling approximately 3.5 years; 2) The length of ‘drug-free interval’ used to ascertain drug discontinuation influences the observed magnitude and significance of comparative persistence estimates; 3) Physician factors (prescribing habits) are predictors and possible confounding factors in studies of persistence and comparative persistence. Conclusions: This thesis provides evidence showing that researchers and physicians can influence estimated and actual comparative persistence on TNFα antagonists in RA patients. The role of researchers and physicians in affecting estimates of persistence may explain heterogeneity in these estimates across different studies. Improved methodology in conducting comparative persistence research is needed to establish a high quality body of evidence for the use of patients, clinicians, researchers and policy makers.

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18

Barsacchi, Rico. "Role of nitric oxide in the regulation of tumor necrosis factor alpha signalling." Thesis, Open University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252359.

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19

Kumari, Vandana. "Mechanisms underlying the regulatory function of tumor necrosis factor-alpha in skin inflammation." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17389.

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Die Haut ist das größte Organ des Menschen und bildet die Barriere gegenüber Einwirkungen aus der Umwelt. Die Störung der Hautbarriere durch exogene und endogene Reize führt zu einer Entzündungsreaktion in der Haut. In der Folge können Hauterkrankungen wie die irritative oder Atopische Dermatitis entstehen. Der Tumor Nekrose Faktor-α (TNF-α) ist ein pleiotrop wirksames Zytokin, das eine zentrale Rolle bei entzündlichen Prozessen spielt. Ziel der vorgelegten Promotionsarbeit war zu untersuchen, ob und wie TNF-α zu Entzündungsgeschehen, ausgelöst durch exogene und endogene Faktoren, beiträgt. Die Bedeutung von TNF-α wurde in TNF-ko Mäusen in verschiedenen Hautmodellen untersucht. Für das Irritationsmodell wurden chemische und physikalische Reize verwendet. TSLP (Thymic stromal lymphopoietin) wurde durch die verschiedenen Stimuli signifikant induziert. Diese Induktion war unabhängig von der endogenen TNF-α Produktion, gezeigt durch den Einsatz von TNF- ko Mäusen . Da endogenes TNF-α für die Hautirritation keine notwendige Bedingung darstellte, wurde die Bedeutung von TNF-α bei der atopischen Dermatitis (AD) untersucht. TNF-α defiziente Mäuse zeigen verstärkt Ekzeme im Vergleich zu Wildtyp Mäusen. Die Behandlung von TNF-ko Mäusen mit einem TSLP Antikörper führte zu einer Verminderung des Ekzems. Mastzellen wurden vermehrt in läsionaler Haut gefunden und korrelierten mit dem Schweregrad des atopischen Ekzems sowie der TSLP-Expression.
The skin is the largest organ of an individuum and builds the barrier for a host against the environment. Skin barrier disruption by exogenous or endogenous stimuli can lead to skin inflammation. As a consequence, irritant or atopic eczema, frequent skin diseases, may evolve. Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine which plays a central role in inflammatory processes. The main aim of this thesis was to clarify whether and how endogenous TNF-α is contributing to skin inflammation driven by exogenous and endogenous triggers. The role of endogenous TNF-α was studied using TNF knockout (-/-) mice. In an irritation model, chemical and physical stimuli were applied on to mouse skin. Thymic stromal lymphopoietin (TSLP) was significantly induced by the used irritants. This TSLP induction was independent from endogenous TNF-α proven by using TNF-/- mice. Next the role of TNF-α in atopic dermatitis (AD) promoting an allergic skin inflammation was investigated. TNF-/- mice developed more severe AD compared to the wildtype mice and TSLP was significantly increased and correlated with the severity of the eczema. To prove the pathophysiological role of TSLP for AD progression, TNF-/- mice were pretreated with an TSLP antibody. Indeed, these mice developed less AD symptoms compared to the control mice. Mast cells (MCs) were also significantly increased in lesional skin in the AD model and moreover, correlated with AD severity, but also with TSLP expression.

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20

Freese, Christiane. "Rolle der Plasmakonzentrationen von transforming growth factor-[beta]1 [factor-beta1] (TGF[beta]1) [TGF beta 1], Tumor necrosis factor [alpha] [Tumor necrosis factor alpha] (TNF [alpha]) [TNF alpha] und Plasminogen-Activator-Inhibitor-(PAI-)-Antigen bei Patienten mit Diabetes Mellitus Typ 2 und koronarer Herzkrankheit." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=97149200X.

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21

Abdo, Michael A. "Tumour necrosis factor : alpha signal transduction in rat corpus luteum apoptosis." University of Western Australia. School of Anatomy and Human Biology, 2002. http://theses.library.uwa.edu.au/adt-WU2003.0024.

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[Formulae and special characters can only be approximated here. Please see the pdf version of the abstract for an accurate reproduction.] Apoptosis is a morphologically distinct form of cell death that is involved in the regulation of normal and aberrant cell systems. The complexities of the apoptotic cell death pathway arise from variation in both the cellular specialisation and initial stimulus. The corpus luteum (CL) is an endocrine gland that whilst critical to the maintenance of pregnancy in the rat, regresses at the completion of each oestrous cycle and pregnancy. This regression is facilitated through apoptosis; though, the stimulus and factors involved in the apoptotic pathway are poorly understood. Previous studies suggest that CL regression is not initiated through failure of luteotrophic support, but rather the active production of a luteolytic factor, of which tumour necrosis factor -alpha (TNFα) is one possible candidate. Several publications have reported the participation of the immune system in ovarian events. There is evidence that TNFα expression within the ovary is coordinated between cells of the immune system and the hormonal regulation of the CL. This study has focussed on the role of TNFα in CL apoptosis and the factors involved in this apoptotic pathway. TNFα-induced cell death is governed by the presence of the two TNFα receptors (TNFR) and several second messenger systems that include; the sphingolipids, mitogen-activated protein (MAP) kinases, nitric oxide (NO), nuclear factor-kappaB (NF-κB) and the caspases. These factors and their interactions were assessed in the rat CL during pregnancy and post-partum, and in vitro. Apoptosis was measured through the analysis of DNA fragmentation using DNA 3’ end labelling and single cell electrophoresis (COMET assay). Assessment of mRNA and protein expression was through Real-time RT-PCR and Western blot analysis; proteins were localised within the CL by immunocytochemistry. In addition, specific measurement of sphingolipid expression and nitric oxide (NO) production was by high performance liquid chromatography (HPLC) and NO assay respectively. Following parturition, TNFα mRNA and protein expression increased corresponding to the onset of CL apoptosis and increased expression of the chemotactic factor monocyte chemoattractant protein -1 (MCP-1). Furthermore, CL apoptosis was induced by treatment with recombinant TNFα in a time- and dose-dependent manner. A similar effect was observed in isolated luteal cells. Simultaneously, the functional regression of the CL was assessed by measurement of both progesterone synthesis and steroidogenic acute regulatory (StAR) protein expression. StAR mRNA and protein expression declined toward parturition in vivo. Immunocytochemical studies revealed the presence of TNFα receptors 1 (TNFR1) and 2 (TNFR2) in luteal cells. Furthermore, TNFR mRNA was isolated from CL throughout pregnancy and post-partum. Subsequently, the role of the sphingolipids ceramide and sphingosine was examined during CL apoptosis in vitro. Ceramide and sphingosine were found to be potent apoptotic agents when administered in vitro (50µM). The downstream signal transduction of TNFα and ceramide was assessed through MAP kinase expression. Both TNFα and ceramide increased expression of the pro-apoptotic p38 MAP kinase with no change to the non-apoptotic extracellular signal-related kinase (ERK1&2). Despite previous reports of c-Jun NH2 terminal kinase (JNK) involvement in the cell death pathway, JNK expression was not evident in the rat CL. The caspases are a family of cysteine proteases central to the regulation and execution of apoptosis. General inhibition of the caspase cascade in vitro was effective in preventing apoptosis regardless of the apoptotic stimulus (TNFα, ceramide and sphingosine), suggesting that this pathway is central to CL apoptosis. Specific inhibition of several caspases produced a varying effect; inhibition of caspases 3, 6 and 8 significantly reduced the level of TNFα-induced apoptosis, thus supporting their classification as either regulatory or effector caspases. NO is endowed with the unique ability to initiate and to block apoptosis and this dichotomy extends to the cytotoxic actions of TNFα. Inhibition of NO production by treating CL with L-NAME prevented the onset of apoptosis, whilst NO production increased in response to increasing levels of apoptosis following trophic withdrawal. However, this effect was not seen during TNFα-induced apoptosis, suggesting that the actions of NO are independent of TNFα. The data presented within this study examine multiple elements of the TNFα cell death pathway in a single system. The results suggest that these elements are involved in TNFα signal transduction and furthermore, in rat CL apoptosis. It can be said that TNFα plays an active role in CL regression through the activation of the caspases, the sphingolipids and the MAP kinases.

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22

FOUQUERAY, BRUNO. "Choc endotoxinique : mecanismes de regulation de la production glomerulaire de tumor necrosis factor alpha." Paris 6, 1996. http://www.theses.fr/1996PA066776.

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Le tumor necrosis factor-alpha (tnf-) est responsable de la majorite des effets du choc endotoxinique mais son role dans la constitution des lesions renales est mal connu. Cette these regroupe quatre etudes dont le but a ete de preciser l'origine cellulaire du tnf dans le glomerule, et surtout les mecanismes responsables du controle de sa synthese. Au cours du choc endotoxinique experimental chez le rat, les cellules glomerulaires residantes contribuent a la synthese renale de cytokines qui comprend le tnf- puis l'interleukine-6 sans generation intermediaire d'il-1. Cette synthese de cytokines est susceptible de modifier l'hemodynamique glomerulaire et l'equilibre de la reaction inflammatoire soit directement, soit par la synthese en cascade d'autres mediateurs de l'inflammation. Le tnf- synthetise est exprime a la membrane des cellules mesangiales de rat avant d'etre libere dans le milieu par un mecanisme faisant intervenir les derives reactifs de l'oxygene. Ceux-ci facilitent la liberation systemique du tnf- et peuvent ainsi concourir a l'aggravation des lesions observees. Le tnf- etant pyrogene, nous avons ensuite analyse in vitro le role du choc thermique sur la production de tnf- par les macrophages tissulaires en particulier glomerulaires et les monocytes circulants. Les resultats indiquent que l'elevation de temperature limite la liberation de tnf- par ces cellules. Il s'agit d'un effet portant sur l'expression du gene et lie a l'induction de proteines du choc thermique. L'interleukine-10 inhibe la production de cytokines proinflammatoires par les monocytes/macrophages. Nous avons mis en evidence sa synthese par les cellules mesangiales de souris exposees au lps et montre que de facon autocrine et paracrine, elle inhibe la liberation de tnf-. La surexpression glomerulaire d'interleukine-10 peut donc representer un mode de controle de la production locale de tnf- dans les situations ou le role toxique de cette cytokine a ete demontre.

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23

Ayub, Qasim. "Prevention of endotoxic shock in mice using anti-tumor necrosis factor-alpha monoclonal antibody." Thesis, University of North Texas, 1991. https://digital.library.unt.edu/ark:/67531/metadc798464/.

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24

Scott, Alasdair James. "The regulation of tumor necrosis factor-alpha converting enzyme (TACE/ADAM17) during acute inflammation." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6041.

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The systemic inflammatory response syndrome (SIRS) describes the immune response to an insult that is inappropriate for a patient’s biological needs. Tumour necrosis factor-α (TNF) is one of the principal pro-inflammatory cytokines that mediates SIRS. TNF-α converting enzyme (TACE) is responsible for the ectodomain cleavage of numerous immunologically relevant substrates including TNF, both TNF receptors and the cellular adhesion molecule L-selectin. The biological significance of TACE lays in its ability to control the availability of these key mediators of the immune response in their membrane-bound and soluble forms. Little is known concerning the regulation of TACE-mediated ectodomain shedding and it contributes to disease pathophysiology. Our objective was to investigate the regulation of TACE catalytic activity and expression during acute inflammation in vitro and in vivo. Our aims were: 1) define the pathways mediating upregulation of TACE activity in primary human monocytes; 2) compare the regulation of TACE catalytic activity and TACE substrate shedding; 3) investigate the acute inflammatory response in elective surgical patients with particular focus on three potential biomarkers of inflammation: TACE expression, HLA-DR expression and circulating monocyte subset populations. We used a fluorimetric assay of TACE activity to demonstrate that lipopolysaccharide (LPS) stimulation of primary human monocytes promotes rapid upregulation of TACE activity, independently of changes in TACE expression. TACE activity upregulation was mediated by reactive oxygen species-induced activation of the p38 MAPK-MK2 pathway. Dithiol oxidation was found to induce L-selectin shedding but to attenuate LPS-induced TACE activity upregulation. Investigation of this paradox revealed that L-selectin shedding may be independent of TACE activity upregulation. Monocyte TACE expression was not modified by low to intermediate risk surgery. In contrast, surgery resulted in downregulation of monocyte HLA-DR expression and differential trafficking of monocyte subsets. These data provide insight into the regulation of TACE during acute inflammation.

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25

Berry, Mark P. McMurray Robert G. "The effect of exercise in the heat on circulating tumor necrosis factor-[alpha] concentration." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1878.

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Thesis (M.A.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Master of Arts in the Department of Exercise and Sport Science Exercise Physiology." Discipline: Exercise and Sports Science; Department/School: Exercise and Sport Science. On t.p. and in abstract, [alpha] is Greek letter.

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26

Ano, Monfils Nadhia. "Etude de la production et des caracteristiques biologiques du tnf alpha humain produit a partir d'une lignee cellulaire humaine." Lillle 2, 1993. http://www.theses.fr/1993LIL2P256.

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27

Gallea, Sylvie. "Le facteur de necrose tumorale alpha humain : identification d'activites proteolytiques impliquees dans sa maturation." Paris 5, 1997. http://www.theses.fr/1997PA05N095.

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28

Pistilli, Emidio E. "The extrinsic apoptotic pathway in aged skeletal muscle roles of tumor necrosis factor-[alpha] and interleukin-15 /." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4912.

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Thesis (Ph. D.)--West Virginia University, 2006.
Title from document title page. Document formatted into pages; contains x, 189 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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Karim, Bahija. "Anticorps monoclonaux murins anti-tnf alpha humain : production, caracterisation et applications." Lille 2, 1993. http://www.theses.fr/1993LIL2P262.

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30

Tillie-Leblond, Isabelle. "Liberation de tnf alpha d'origine mastocytaire au cours des reactions systemiques dans l'urticaire au froid." Lille 2, 1993. http://www.theses.fr/1993LIL2M193.

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31

Hober, Didier. "Etude du tumor necrosis factor alpha chez des sujets infectes par le virus de l'immunodeficience humaine." Lille 2, 1989. http://www.theses.fr/1989LIL2M024.

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32

Phillips, Tracey. "Effects of age and calorie restriction on tumor necrosis factor-alpha signaling in skeletal muscle." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0004283.

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33

Simon, Fabrice. "Tumor necrosis factor alpha et paludisme : etude sérologique du TNF alpha dans 41 observations de paludisme à Plasmodium falciparum." Bordeaux 2, 1990. http://www.theses.fr/1990BOR25211.

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34

Caron, Emmanuelle. "Etude de l'interaction "Brucella"/macrophage humain : implication du TNF alpha (Tumor Necrosis Factor alpha) dans le contrôle de l'infection." Montpellier 2, 1994. http://www.theses.fr/1994MON20273.

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La brucellose atteint l'homme et les animaux d'elevage. Son agent etiologique, brucella, est une bacterie gram-negative a multiplication intramacrophagique. Nous avons developpe un modele experimental d'interaction entre pathogenes intramacrophagiques et macrophage humain, base sur l'utilisation de cellules de la lignee u937, differenciees en macrophages in vitro. Dans ce modele, listeria monocytogenes brucella melitensis, et certains biovars de b. Suis, pathogenes pour l'homme, se multiplient dans les macrophages, alors que l. Ivanovii, pathogene animal, est eliminee. L'opsonisation des brucelles ou l'activation des cellules par le tnf alpha (mais pas l'ifn gamma) reduit la multiplication intracellulaire de b. Suis. Contrairement a l'infection de cellules murines, l'infection des macrophages humains par brucella ne s'accompagne pas de la liberation de tnf alpha. En revanche, les brucelles tuees sont capables d'induire la secretion de tnf alpha. Brucella inhibe la liberation de tnf alpha induite dans les macrophages. Cette propriete repose sur l'existence d'un facteur soluble, libere par brucella lors de son interaction avec le macrophage. Ce facteur, present dans les surnageants de culture de brucella, est capable d'inhiber specifiquement la liberation de tnf alpha par les macrophages humains, mais n'est pas actif sur les macrophages murins. Plusieurs arguments suggerent que ce facteur pourrait constituer un facteur de virulence pour brucella

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35

Terry, Jennifer L. "The characterization of TRUSS : a novel scaffolding protein in tumor necrosis factor-[alpha] receptor-1 signaling /." Connect to full text via ProQuest. IP filtered, 2005.

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Thesis (Ph.D. in Immunology) -- University of Colorado, 2005.
Typescript. Includes bibliographical references (leaves 190-212). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

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36

AMRANI, YASSINE. "Role du recepteur p55 au tnfα dans les variations phenotypiques des cellules musculaires lisses des voies aeriennes : implication dans la physiopathologie de l'asthme." Strasbourg 1, 1995. http://www.theses.fr/1995STR15053.

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37

Gure, Ali Osmay. "Analysis of TNF mediated cytotoxicity /." Access full-text from WCMC, 1995. http://proquest.umi.com/pqdweb?did=733006521&sid=10&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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38

Caughey, Gillian Elizabeth. "Regulation of interleukin-1[Beta] and tumor necrosis factor[alpha] synthesis by fatty acids and eicosanoids /." Title page, table of contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phc371.pdf.

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39

Golds, Gary Brandhorst. "Interleukin-10 inhibition of tumor necrosis factor alpha production in activated macrophages requires SHIP1 and Btk." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/26036.

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Inflammation is a physiological process required for defense against pathogens and the repair of damaged tissues. However, excessive or improper inflammation can be detrimental and results in a number of diseases such as rheumatoid arthritis and inflammatory bowel disease. To prevent the negative effects of inflammation, the inflammatory response is tightly regulated by the anti-inflammatory cytokine interleukin-10 (IL-10). The main target of IL-10 are activated macrophages whose exposure to IL-10 results in the anti-inflammatory response (AIR) characterized by depressed antigen presentation and the inhibited secretion of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNFα). To induce the AIR in macrophages, IL-10 binds to cell surface receptors which activate the transcription factor STAT3 leading to the transcription of gene products responsible for carrying out the AIR. However, we hypothesized that IL-10 also uses a STAT3-independent mechanism to induce the AIR. Here we demonstrate that IL-10 utilizes the lipid phosphatase SHIP1 to inhibit TNFα production in activated macrophages. SHIP1 is responsible for dissociating TNFα mRNA from polysomes leading to inhibited translation of TNFα mRNA during the AIR. This effect of SHIP1 occurs early in the AIR and helps to immediately halt TNFα production. We also demonstrate that the tyrosine kinase Btk, a reported positive regulator of TNFα production in macrophages, is also utilized by IL-10 in the early AIR to inhibit TNFα production. However, Btk is not required for IL-10 to dissociate TNFα mRNA from polysomes suggesting that Btk and SHIP1 are involved in distinct IL-10 signalling pathways. Finally we show that TIA-1, a RNA binding protein that silences TNFα mRNA translation is not involved in the IL-10 AIR. These results clearly demonstrate the existence of non-STAT3 signalling pathways in the IL-10 AIR and suggest that SHIP1 and Btk activators could be used as potential therapeutics in the treatment of inflammatory disorders.

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40

Goffette, Nicolas. "Caractérisation des mécanismes de régulation de la synthèse du Tumor Necrosis Factor-alpha par le nicotinamide." Doctoral thesis, Universite Libre de Bruxelles, 2013. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209430.

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Dans le cadre de l’étude de la régulation de la synthèse de la cytokine pro-inflammatoire TNF-alpha dans les cellules myéloïdes stimulées aux lipopolysaccharides, nous avons pu mettre en évidence que l’effet anti-inflammatoire du nicotinamide (NAM) sur la production de cette cytokine s’opère au niveau de l’état de phosphorylation de la MAPK p38. Une diminution de la concentration intracellulaire de NAD entraine également une inhibition de la phosphorylation de la MAPK p38 en réponse aux lipopolysaccharides. De plus, une étude pharmacologique plus ciblée suggère que les sirtuines, une famille d’enzymes consommatrices de NAD, sont impliquées dans cette régulation. Nos résultats indiquent que ce processus s’effectuerait par un contrôle de l’expression des gènes mkp-1 et pac-1 codant pour des « dual-phosphatases » modulant l’état de phosphorylation des MAPKs. Enfin, nos données indiquent que l’effet anti-inflammatoire du NAM s’opère aussi par une régulation de l’efficacité traductionnelle du messager du TNF-alpha impliquant un raccourcissement de la queue poly(A) du messager. En conclusion, l’ensemble de nos données montre une complexité importante dans la régulation de la production de TNF-alpha dans les cellules myéloïdes par des enzymes consommatrices de NAD, dont les sirtuines.
Doctorat en sciences, Spécialisation biologie moléculaire
info:eu-repo/semantics/nonPublished

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41

Osta, Bilal. "Effects of Interleukine-17A (Il-17A) and tumor necrosis factor alpha (TNF-α) on osteoblastic differentiation." Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10278/document.

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L'interleukine-17A (IL-17A) et le facteur de nécrose tumorale alpha (TNF-α) sont des cytokines pro-inflammatoires impliquées dans la pathogénèse de plusieurs maladies articulaires. Au cours de la polyarthrite rhumatoïde (PR), une augmentation de la destruction osseuse ainsi qu'un defaut de réparation sont responsables des dommages articulaires. Cependant au cours de la spondylarthrite ankylosante (AS), une importante ossification ectopique est observée, conduisant à la formation de syndesmophytes, associé à une perte de la masse osseuse systémique. Récemment, l'étude de ces cytokines a conduit à la publication de résultats contradictoires. Notre objectif a donc été d'étudier l'effet de ces deux cytokines sur la différenciation ostéogénique de cellules souches mésenchymateuses humaines isolées (hMSCs) et de fibroblastes de la membrane synoviale (FLS). Tous les modèles de cellules utilisés, ont démontré que l'IL-17A et le TNF-α augmentent de manière synergique l'ostéogénèse. Ceci semble se rapprocher du modèle de l'AS où une formation d'os ectopique est observée dans laquelle l'IL-17A et le TNF-α jouent un rôle majeur. En parallèle, ces deux cytokines stimulent localement les ostéoclastes, entraînant une perte de masse osseuse observée à la fois dans la PR et dans l'ostéoporose. Cibler simultanément l'IL-17A et le TNF-α pourrait conduire à une diminution de l'infiltration de cellules et de la destruction articulaire observée dans la PR et pourrait ainsi réduire les effets des FLS PR sur l'activation de l'ostéoclastogénèse
Interleukin-17A (IL-17A) and tumor necrosis factor alpha (TNF-α) are pro-inflammatory cytokines involved in the pathogenesis of several arthritic diseases. In rheumatoid arthritis (RA), joint damage is a result of an increase in bone destruction and a decrease in bone repair. In contrast, in ankylosing spondylitis (AS), a bone mass loss accompanied by a significant ectopic ossification is observed leading to the formation of syndesmophytes. Recent studies led to contradictory findings regarding the role of IL-17A and TNF-α in arthritic disease. Therefore, our objective was to study the effect of these two cytokines on the osteogenic differentiation of isolated human mesenchymal stem cells (hMSCs) and fibroblasts of the synovial membrane (FLS). In all the cell models used, we demonstrated that Il-17A and TNF α synergistically increase osteogenesis. This seems to approach the model of AS where ectopic bone formation is observed and in which IL-17A and TNF-α both are involved. These cytokines stimulate osteoclasts locally resulting in loss of bone mass observed in both RA and osteoporosis. Thus, targeting IL-17A and TNF-α could lead to a decrease in cell infiltration and joint destruction which is observed in RA and may reduce the effects of RA FLS on the activation of osteoclastogenesis

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42

Medina, Edward Antonio. "Tumor necrosis factor-alpha and insulin interactions : effects on leptin production and Akt expression in adipocytes /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.

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43

Balga, Renate. "Tumor necrosis factor-alpha in bone loss induced by ovariectomy and in the development of osteoclasts /." [S.l.] : [s.n.], 2004. http://www.zb.unibe.ch/download/eldiss/04balga_r.pdf.

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44

Beck, Eichler-Jonsson Claudia. "Aspects of mitogen activated protein kinase cascade activation by epidermal growth factor (EGF) kinetics and crosstalk mechanism with tumor necrosis factor [alpha] (TNF[alpha]) /." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965959937.

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45

Kostyk, Amanda Gail. "Tumor necrosis factor-[alpha] : a critical cytokine at the crossroads of fibrosis and inflammation in the lung /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.

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Thesis (Ph.D. in Immunology) -- University of Colorado at Denver and Health Sciences Center, 2006.
Typescript. Includes bibliographical references (leaves 182-208). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

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46

Cartwright, Megan. "Down-regulation of tumor necrosis factor-alpha in Dunkin-Hartley guinea pig chondrocytes using RNA interference techniques." Connect to resource, 2006. http://hdl.handle.net/1811/6563.

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Thesis (Honors)--Ohio State University, 2006.
Title from first page of PDF file. Document formatted into pages: contains 19 p.; also includes graphics. Includes bibliographical references (p. 17-19). Available online via Ohio State University's Knowledge Bank.

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47

Piéroni, Laurence. "Sécrétion d'érythropoi͏̈étine au cours des anémies inflammatoires chez le sujet âgé : influence du Tumor Necrosis Factor alpha." Paris 5, 1993. http://www.theses.fr/1993PA05P034.

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48

Mauduit, Claire. "Le tumor necrosis factor alpha est un inhibiteur de l'action des gonadotrophines sur les fonctions gonadiques mâles." Lyon 1, 1993. http://www.theses.fr/1993LYO1T277.

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49

Bergman, Marina R. "Pharmacological modulation of myocardial tumor necrosis factor (alpha) secretion by phosphodiesterase inhibitors in heart failure prone rats /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487940665437311.

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50

Buck, Isabelle. "Molecular mechanisms leading to the inhibition of erythroid differentiation by the proinflammatory cytokine tumor necrosis factor alpha." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:16-opus-87528.

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