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1
Patrikainen, Lila. "Prostatic gene expression : probasin, human prostatic acid phosphatase and macrophage inhibitory cytokine-1 as model genes /". Oulu : Oulun yliopisto, 2004. http://herkules.oulu.fi/isbn9514272730/.
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Patrikainen, L. (Lila). "Prostatic gene expression: probasin, human prostatic acid phosphatase and macrophage inhibitory cytokine-1 as model genes". Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514272730.
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Abstract
Gene products that are only expressed in one tissue or cell type are useful models for investigating the biochemical and molecular mechanisms of tissue/cell-specific gene regulation. The regulatory regions of such genes are also practical tools in gene therapy.
In this work, prostate-specific and androgen-dependent gene regulation was investigated by using human prostatic acid phosphatase (hPAP) and rat probasin (rPB) as models. In DNase I footprinting, a protected 12 bp region was found in the PB gene between the nucleotides -251 and -240 only with nuclear extracts of prostatic origin. The sequence of this area was GAAAATATGATA. Weak interaction could be detected between the DNA-binding domain of AR and the prostatic transcription factor. The results also suggested that the prostatic regulatory protein makes AR binding to its response element more effective and concomitantly magnifies the effect of androgen.
A hPAP construct containing the sequence between the nucleotides -734 and +467 in front of the CAT reporter gene was highly expressed in the prostate of transgenic mice. Five homologues (A-E) for our previously identified prostate-specific GAAAATATGATA DNA-binding site were found in the area where the sites C and E could bind the regulatory protein in EMSA.
The prostatic transcription factor complex bound to the GAAAATATGATA site was purified and characterized from a suspension-adapted mass culture of PC-3 prostate cancer cells by using sequence-specific DNA affinity chromatography, mass spectrometry and supershifts. Several potential transcription factors were identified, but only USF2 was confirmed to be part of the transcription factor complex.
Two PC-3 cell line variants (anchorage-dependent and suspension-adapted, anchorage-independent variants) were used as a model for advanced, androgen-independent prostate cancer. Genes that were overexpressed in a suspension-adapted PC-3 cell line were further investigated, since they can be considered as putative markers of metastatic activity. The macrophage inhibitory cytokine-1 (MIC-1) gene, which was overexpressed in the suspension-adapted PC-3 cell line, was further investigated in order to clarify the mechanism behind aggressive cell growth and androgen-independent gene regulation. In patient specimens, MIC-1 had no or low expression in benign prostatic hyperplasia and normal prostate but high in prostatic cancer and therefore it could be a useful marker for aggressive prostate cancer. Indomethacin increased the expression of MIC-1 in PC-3 cells, and apoptosis was also induced in this cell line but not in saPC-3 cell line suggesting a block in MIC-1 inducible apoptosis pathway.
3
Rasiah, Krishan Kumar St Vincent's UNSW. "The identification of novel biomarkers in the development and progression of early prostate cancer". Awarded by:University of New South Wales. St Vincent's, 2006. http://handle.unsw.edu.au/1959.4/24187.
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ABSTRACT The morphological premalignant changes in prostate epithelium such as high grade prostatic intraepithelial neoplasia (HGPIN) precede invasive prostate cancer (PC) by several decades. The overall aim of this project was to identify patterns of gene expression in HGPIN and early PC which increase our understanding of the early biology of PC and identify genes and pathways that correlate with an aggressive phenotype. A comprehensive tissue cohort of premalignant prostate lesions was collected in a tissue microarray (TMA) platform that was utilised for high-throughput validation of target genes. Using this unique resource, the expression of the tumour suppressor gene PTEN was assessed using immunohistochemistry in an initial candidate gene approach based on mouse models implicating PTEN in carcinogenesis. No significant difference in expression of PTEN was detected in premalignant and benign epithelium. A transcript profiling approach was undertaken by integrating laser capture microdissection, linear RNA amplification and oligonucleotide microarrays to perform a screen of matched patient samples of normal, HGPIN and PC cells. The expression patterns of two genes encoding secreted proteins, neuropeptide Y (NPY) and macrophage inhibitory cytokine (MIC-1) were validated using immunohistochemistry on TMAs representing the progression model of early PC. Increased expression of these proteins in PC was confirmed to occur early in the disease process and altered expression of NPY and MIC-1 was associated with worse clinical outcome. Further analysis of global gene expression patterns using a structured network knowledge base identified a notable aberration in the expression of extracellular matrix and extracellular matrix associated proteins in HGPIN and provided novel evidence for the role of this class of molecules in the development of PC. In summary, contrary to current dogma based on work in animal models, altered PTEN expression is unlikely to represent an important event in the development of malignancy in the human prostate. In contrast, the expression patterns and prognostic value of NPY and MIC-1 in HGPIN support their further evaluation as biomarkers for the development and progression of PC. The aberrant expression of genes and networks of genes detected in HGPIN will assist in further identification of biological pathways which may be targeted in therapeutic strategies against the development and progression of PC.
4
Montero, Rosa Maria. "Chemokines and macrophage migration inhibitory factor in diabetic nephropathy". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29851.
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Introduction: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease in the Western world. Aim: To determine whether macrophage migration inhibitory factor (MIF), monocyte chemoattractant protein-1 (MCP-1) or CC chemokine ligand 18 (CCL18) have a causative role in the development of renal inflammation and fibrosis in DN and are useful biomarkers of disease progression. Methods: Urine and plasma samples were collected from 115 DM and 116 Non-DM at baseline, previously analysed for MCP-1 and CCL18 ELISA by Dr Qureshi. I measured MIF in these samples and collected 107 DM and 114 Non-DM data points (GFR, ACR/UPCR and clinical parameters) at >18 months and >3 years. MIF, MCP-1 and CCL18 urine, plasma and serum analysis was performed in 42 DM and 60 Non-DM at >3 years follow up. Intrinsic renal cells were cultured and stimulated with diabetic conditions. These cytokines and fibronectin were measured in tubuloepithelial cells and podocytes. Results: Baseline plasma CCL18 and MIF predicted a decline in GFR in DM at >18 months but not at >3 years. Cytokine production varies over time with significant correlations at baseline that are not maintained. Cytokines correlate differently with GFR, ACR/UPCR in DM versus Non-DM proteinuric renal diseases. Plasma and serum cytokine levels correlated significantly with no correlation between these and urinary levels. All intrinsic renal cells were able to produce MIF, MCP-1 and CCL18 following stimulation. The interaction of these cytokines and their effects on fibronectin vary in diabetic conditions and following recombinant cytokine stimulation. The diabetic environment appears to orchestrate cytokine signals according to cell type. Conclusion: These results suggest cytokines may play a key role in the pathogenesis and or progression of DN. The clinical study suggests cytokines may predict progression; however, larger studies are needed with samples taken at different time points.
5
Powell, Nicole Damico. "Immunomodulation of experimental autoimmune encephalomyelitis targeting the autoreactive T cell and the cytokine macrophage migration inhibitory factor /". Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141052089.
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Russell, Kirsty. "The role of macrophage migration inhibitory factor in airways disease". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/23917.
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Chronic obstructive pulmonary disease (COPD) and severe asthma are progressive chronic inflammatory diseases of the airways. Both diseases are characterised by airflow limitation and share some pulmonary symptoms. However they have distinct inflammatory cell signatures and differ in response to corticosteroid (CS) treatment. Most asthmatic patients control their disease with CS, with a few showing a relative CS resistance; however COPD patients show little or no improvement with CS and are CS insensitive. Macrophage migration inhibitory factor (MIF) is a pleiotropic pro-inflammatory mediator whose function is yet to be fully elucidated. MIF has been shown to counter-act the immunosuppressive action of CS. MIF is elevated in chronic diseases such as asthma and atherosclerosis. The role of MIF in COPD has not been investigated and its role in asthma is not fully understood. MIF inhibition attenuated ozone-induced airway inflammation and lung function in vivo but did not affect CS sensitivity. MIF expression did not vary between stable COPD patients and controls. Pro-inflammatory effects of MIF were investigated in THP-1 monocytes and primary cells. There was no clear role for MIF in LPS-induced inflammation. MIF modulated the transactivation functions of CS in THP-1 cells. Finally I took an unbiased approach to generate new hypotheses for MIF function using proteomic and transcriptomic techniques. The RIG-I-like pathway was identified by proteomics as a novel target pathway and was investigated in THP-1 cells and human BAL macrophage samples following viral infection. The role of MIF in airway inflammation remains unclear and results demonstrated here show MIF function does not necessarily translate from mouse to humans. MIF does not seem to have a role in the inflammation of stable disease. The proteomic data suggests that the association between viral infection, MIF and CS in regulating CS sensitivity in COPD and severe asthma should be investigated.
7
Nguyen, Tuyet Mai. "Elucidation of thiol-protein oxidoreductase activity of the cytokine macrophage migration inhibitory factor (MIF) by biochemical redox and site-specific mutagenesis analysis". [S.l. : s.n.], 2003. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10520514.
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Liu, Yu. "The role of suppressors of cytokine signalling 1 and 3 in macrophage activation". Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24848.
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Baeza, Garcia Alvaro. "Rôle de MIF (Macrophage Migration Inhibitory Factor) dans l'immunité innée et la réponse anti-schistosome chez Biomphalaria glabrata". Phd thesis, Université du Droit et de la Santé - Lille II, 2010. http://tel.archives-ouvertes.fr/tel-00665113.
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Schistosoma mansoni est un parasite helminthe responsable de la schistosomiase intestinale, qui affecte 200 millions de personnes dans les zones tropicales et subtropicales, et l'on estime que 600 millions de personnes sont exposées au risque de cette infection. Le cycle de vie du parasite est complexe et il requière, un hôte définitif, l'homme et un hôte intermédiaire, un mollusque d'eau douce appelé Biomphalaria glabrata. C'est chez le mollusque où le parasite se multiplie de forme massive de là l'importance du mollusque dans la transmission du parasite à l'homme. Lors de l'infection le mollusque met en place une réponse cellulaire et humorale très marquées pouvant dans certains cas tuer le parasite. Malgré l'importance du mollusque, les mécanismes moléculaires qui gouvernent ces réponses sont largement inconnus et donc l'étude de l'immunité du mollusque est une priorité en recherche médicale. Nous avons identifié deux orthologues de la cytokine de mammifère MIF (Macrophage Migration Inhibitory Factor ) BgMIF1 et BgMIF2. En utilisant des approches biochimiques et moléculaires en combinaison avec la technique de RNAi in vitro et in vivo nous avons démontré le rôle de BgMIF 1 et BgMIF2 comme régulateurs centrales de l'immunité innée du mollusque. En particulaire BgMIF1 régule l'activation des hémocytes et la réponse d'encapsulation lors de l'infection. D'un autre côté BgMIF2 régule dans la réponse antibactérienne. Nos résultats montrent que chez B. glabrata il y une régulation fine de la réponse immune innée et une capacité pour répondre de façon différente lors d'un challenge immunitaire. De plus une régulation par une cytokine de type vertébré dans un invertébré n'avait jusqu'à présent jamais été décrite. Nos travaux établissent les bases pour mieux comprendre les relations hôte-parasite dans une maladie comme la schistosomiase, et aussi constituent une avancée importante du point de vue de l'évolution de l'immunité innée en général.l
10
Tamaki, Hiroyuki. "Human thioredoxin-1 ameliorates experimental murine colitis in association with suppressed macrophage inhibitory factor production". Kyoto University, 2007. http://hdl.handle.net/2433/135755.
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Nicaise, Pascale. "Effets modulateurs de la flore intestinale sur les marqueurs membranaires et la production de cytokines (il-1, il-6, tnf alpha et il-12) de macrophages de souris (doctorat : microbiologie)". Paris 11, 1998. http://www.theses.fr/1998PA114844.
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Baía, Diogo Nogueira de Graça 1984. "Role of the LILRB1 HLA class I-specific inhibitory receptor in the regulation of macrophage function". Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/380898.
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In the present work the regulatory role played by the HLA class I (HLA-I)-specific LILRB1 inhibitory receptor in human macrophages (MΦ) was addressed. In vitro differentiated monocyte-derived M1 and M2 MΦ expressed different LILRB1 levels. We provide experimental evidence supporting that LILRB1-HLA-I interaction regulated the MΦ activation threshold, controlling cytokine secretion under steady state as well as in response to tumor cells and to signaling through activating receptors. On the other hand, our observations support that LILRB1 binding to cells occurred independently of total HLA-I expression levels, correlating with HLA-I dimerization. Such conformational change was detectable in type I IFN-treated MΦ and associated to an enhanced LILRB1-HLA-I interaction, thus providing a potential regulatory mechanism to control MΦ activationEn aquest projecte hem analitzat la participació del receptor inhibidor específic per HLA de classe I: LILRB1, en la regulació de la funció dels macròfags humans (MΦ). Els macròfags M1 i M2 diferenciats in vitro expressen nivells diferents de LILRB1. Aportem evidències experimentals que recolzen el paper de la interacció LILRB1/HLA-I com element regulador del llindar d’activació en la homeòstasi del macròfag, influint en la secreció de citocines en condicions basals així com en resposta a cèl.lules tumorals i a la senyalització de receptors activadors dependents de motius ITAM. D’altra banda, les nostres observacions indiquen que el reconeixement de cèl.lules diana per part de LILRB1 es dóna independentment del nivell d’expressió de les molècules del HLA en la seva superfície, però correlaciona amb la dimerització d’aquestes molècules. Aquest canvi conformacional, detectat en MΦ tractats amb interferons de tipus I, s’associa a un increment de la interacció entre LILRB1 i HLA-I, suggerint un possible mecanisme regulador de l’activació del MΦ.
13
Praloran, Vincent. "Etude du csf-1 dans la pathologie hematolymphoide : analyse de la production lymphocytaire t et sa regulation". Nantes, 1991. http://www.theses.fr/1991NANT04VS.
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Karathanos, Athanasios [Verfasser], i Tobias [Akademischer Betreuer] Geisler. "Macrophage migration inhibitory factor and gremlin-1 in patients with coronary artery disease and diabetes : patterns of expression and interaction / Athanasios Karathanos ; Betreuer: Tobias Geisler". Tübingen : Universitätsbibliothek Tübingen, 2018. http://d-nb.info/1196701288/34.
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Pons, Isabelle. "Synthèse des cytokines proinflammatoires et expression des molécules d'adhérence par le monocyte/macrophage humain irradié". Paris 5, 1997. http://www.theses.fr/1997PA05S027.
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Les évènements pathologiques précoces apparaissant après exposition aux rayonnements sont caractérisés essentiellement par l'activation et la sécrétion de substances vasoactives et inflammatoires impliquées dans le déclenchement et l'entretien de la réaction inflammatoire locale et systémique. Certaines de ces réactions peuvent devenir délétères principalement quand leur stimulation est excessive et qu'elle conduit à des réactions secondaires sans régulation appropriée. La persistance de monocytes/macrophages radiorésistants au sein des sites irradies pourrait etre une des causes d'apparition des lésions radio-induites. Nous avons donc étudié, in vitro l'effet de l'irradiation sur l'expression et la sécrétion des cytokines proinflammatoires par le monocyte/macrophage humain. Aucune modulation significative de l'expression des arnm et de la sécrétion du tnf, de l'il-1 et de l'il-6, n'a été détectée, entre 30 mn et 7 jours post-irradiation, pour cinq donneurs sur les sept testes ; en effet, deux donneurs ont présenté une augmentation, respectivement d'un facteur 5 et d'un facteur 14, du niveau d'expression du gène codant l'il-6, 2 h après l'irradiation (10 gy) des monocytes/macrophages différenciés pendant 24 h. De plus, le donneur présentant la plus forte activation du gène de l'il-6, a répondu à l'irradiation par une élévation significative de la sécrétion de tnf, d'il-1 et d'il-6, entre 30 mn et 24 h. Afin d'appréhender le rôle du microenvironnement cellulaire dans l'inflammation radio-induite, nous avons étudié les conséquences d'une costimulation des monocytes/macrophages par l'irradiation et le lps, ainsi que l'exposition des cocultures de monocytes/macrophages et de lymphocytes autologues à l'irradiation dans leur aptitude à moduler la régulation des cytokines proinflammatoires. Les cellules traitées par 1 g/ml de lps ont répondu à l'irradiation par une augmentation d'expression des arnm de l'il-1 et une inhibition d'expression des arnm de l'il-6. En ce qui concerne la sécrétion, les traitements combines par l'irradiation et le lps, ont conduit, dans la majorité des cas, à une inhibition de la réponse, comparativement aux cellules contrôlés traitées par le lps et non irradiées. En présence de lymphocytes autologues, le niveau d'expression des arnm de l'il-6, dans les cellules irradiées, a été augmenté très légèrement à 2 h et fortement à 24 h. L'irradiation- a induit également un accroissement important des secrétions d'il-1 et d'il-6, au même moment, à 24 h. Par ailleurs, l'apparition d'une inflammation radio-induite implique le recrutement précoce des leucocytes au sein des sites lésés. L'extravasation et l'infiltration tissulaire des leucocytes nécessitent l'interaction de la cellule avec son environnement via les molécules d'adhérence. Ainsi, seuls les donneurs présentant une forte proportion de lymphocytes dans les cultures ont répondu à l'irradiation- par une augmentation de la sous-unité 1 (cd29) et une diminution de la sous-unité 2 (cd18) à la surface cellulaire, et ceci quel que soit l'état de différenciation du monocyte/macrophage. Au total, dans notre système expérimental, l'irradiation- in vitro, des monocytes/macrophages a entrainé des modulations d'expression des molécules d'adhérence et de la synthèse des cytokines proinflammatoires, essentiellement en présence de lps ou de lymphocytes autologues. En conséquence, le microenvironnement semblerait être l'un des facteurs majeurs des altérations radio-induites.
16
Alexander, Lindsey Ann. "The Role of Inflammation in Diet-Induced Insulin Resistance". University of Toledo / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1260808416.
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Derrien, Danièle. "Modulateur de la réponse immune : ciblage par des polymères glycosyles reconnus par les lectines membranaires des macrophages murins". Orléans, 1988. http://www.theses.fr/1988ORLE2037.
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Realisation d'un vecteur reconnu par les lectrines membranaires des macrophages et destine a transporter le n-acetylmuramyl dipeptide vers ces cellules. L'efficacite de ce vecteur est etudiee in vitro et in vivo sur des modeles murins. L'activation du macrophages a ete evaluee par la cytostase exercee vis-a-vis des cellules tumorales et par la secretion d'interleukine 1 et de facteur de necrose tumorale
18
Chumble, Anuja. "Epigenetic Alterations of Toll-Like Receptors by TET2 in Spontaneous Preterm Labor". VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3469.
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Increasing evidence implicates the presence of bacteria in intrauterine tissues as an important risk factor for spontaneous preterm labor. Epigenetic alterations of innate immunity genes may increase the mother’s sensitivity to subclinical levels of bacteria. This study examined the presence of TET2, TLR-2, and TLR-9 in intrauterine tissue, and evaluated whether epigenetic alterations of these genes, as well as IL-8, changed their expression in human decidual tissue and a macrophage cell culture. Immunohistochemicalstaining was used to detect the presence of these proteins in intrauterine tissue. Gene expression changes were evaluated in stimulated monocytes and macrophages. Fluorescence immunohistochemistry was used to track translocation of TET2 in stimulated monocytes and macrophages. Secreted IL-8 concentration was detected with ELISA. Decidual expression of TET2, TLR-2, and TLR-9 increased in the order TNL < TL < sPTL < iPTL. This study found that TET2, TLR-2, TLR-9, and IL-8 are regulated by epigenetic mechanisms. This study was the first to report activation of TET2 involves its translocation from the cytosol to the nucleus in macrophages.
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Britto, Karen Elma. "The Role of Discoidin Domain Receptor 1 (Ddr1) on Macrophages in Adhesion and Cytokine Production". Thesis, 2010. http://hdl.handle.net/1807/25438.
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Atherosclerosis is an inflammatory disease of the cardiovascular system. Discoidin
domain receptor 1 is a receptor tyrosine kinase that binds collagens. Previous work in our lab has shown that deleting DDR1 in a mouse model results in attenuation of
atherosclerosis, with fewer macrophages in the plaque. The aim of this study was to
determine what changes in macrophage behaviour due to the lack of DDR1 was
attenuating plaque development.
In order to carry out experiments, primary mouse peritoneal macrophages were used.
DDR1-deficient macrophages adhered significantly less to type IV collagen and
fibronectin compared to DDR1-expressing cells. In addition, when plated on type IV
collagen and fibronectin, DDR1-deficient macrophages produced decreased levels of
MCP-1 protein, a cytokine known to be important in plaque development, particularly in leukocyte recruitment to plaque. These results suggest that DDR1 is an important mediator in macrophage adhesion to matrix and macrophage cytokine production
20
Bélanger, Benoît. "La neutralisation du facteur d'inhibition de migration des macrophages (MIF) augmente la sécrétion du TNF-a et module la sécrétion d'IFN-y durant l'infection par plasmodium chabaudi adami". Mémoire, 2008. http://www.archipel.uqam.ca/1475/1/M10597.pdf.
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Le paludisme, une maladie inflammatoire, est caractérisé par une production du facteur de nécrose tumoral (TNF)-α, du facteur d'inhibition de migration des macrophages (MlF) et d'interféron (lFN)-y, qui inhibent les précurseurs érythropoïétiques de la moelle osseuse. Dans ce contexte, le MlF est sécrété durant les infections par Plasmodium, et sa synergie avec l'lFN-y et le TNF-α contribue à inhiber la différenciation érythropoïétiques et la production d'hémoglobine (Hb). Cet travail à démontrer que la neutralisation in vivo du MlF avec un anticorps monoclonal durant l'infection par Plasmodium chabaudi adami DK amène à une diminution du pic de la parasitémie et de façon inattendue à une production accrue de TNF-α en début d'infection et au pic d'infection. La neutralisation du MlF altère la production d'IFN-y et l'IL-10 durant l'infection. Au moment où la parasitémie est faible, une diminution significative de la production d'lFN-y, accompagnée par une chute importante de l'IL-10, est observée dans la rate de souris infectées et traitées avec l'anti-MIF. Par contre, au pic de l'infection, la production de l'IFN-y et l'IL-10 augmente chez les souris traitées avec l'anti-MIF. En plus de ces effets inhibiteurs au pic de l'infection, la neutralisation du MlF entraîne une diminution du pourcentage de réticulocytes en circulation en début d'infection et cet effet est accompagné par une légère diminution des érythrocytes basophiliques (EryA) dans la rate. La concentration d'hémoglobine sanguine était plus élevée chez les souris traitées avec l'anticorps anti-MIF, et ce, au pic de l'infection, ce qui suggère que la neutralisation du MlF, par son effet sur la parasitémie, diminue la destruction des érythrocytes par le parasite. ______________________________________________________________________________ MOTS-CLÉS DE L’AUTEUR : Paludisme, Hémoglobine, Cytokine inflammatoire, MlF, Parasitémie.
21
Li, Chen-yu, i 李晨宇. "Inhibitory effect of microwave radiation on LPS-induced NFκB cytokine expression in the THP-1 monocytes". Thesis, 2010. http://ndltd.ncl.edu.tw/handle/zaw97z.
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碩士元培科技大學
醫學檢驗生物技術研究所
98
Microwave radiations, can be encountered regularly in daily lives. When World Health Organization (WHO) announced that microwave radiations as a kind of environmental energy which interferes with the physiological functions of human body, great concerns have been raised over the damage frequency can do to human physiology. The immunological performance and the activeness of cellular inflammatory factor NFκB have been closely related in monocyte. Due to the effect of phorbol 12-myristate 13-acetate (PMA) to THP-1 monocytes, THP-1 monocytes will divide into macrophages and will then react with lipopolysaccharides (LPS), and the amount of NFκB cytokine increases in THP-1 monocytes. Expression of cytokine will be affected when cells are exposed to frequency at 2450 MHz and are worked at 900W. Thus, from our experiments, an observation can be made when THP-1 monocytes are stimulated with PMA and LPS to differentiate into macrophage, the amount of NFκB cytokine in cells increases exponentially, and the level of expression is also restricted by the exposure of frequency. In conclusion, microwave radiations can inhibit the activity functions of THP-1 monocytes to be stimulated with PMA and LPS.
22
Kao, Yung-Ling, i 高咏菱. "The regulation of polyunsaturated fatty acids (PUFAs) on macrophage migration inhibitory factor (MIF) in THP-1 macrophages". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/65637995210095324682.
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碩士國立陽明大學
生化暨分子生物研究所
100
Macrophage migration inhibitory factor (MIF) is an important pro-inflammatory cytokine and has presumed a vital role as a upstream regulator of host antimicrobial responses. Macrophages act as sentinel cells in the innate immune system. They play roles in destroying pathogens and releasing substances that act on other immune cells. MIF lacks an amino-terminal leader sequence, indicating that it is secreted from cells by a non-classical secretion pathway. Literatures report that MIF is implicated in the pathogenesis of sepsis and inflammatory diseases, suggesting that MIF might offer a therapeutic target for human diseases. Animal experiments and clinical studies demonstrate that n-3 polyunsaturated fatty acids (n-3 PUFAs) might also have the therapeutic effect on anti-inflammation. In this study, THP-1 macrophages were pretreated with docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) for 24 hours before stimulation with LPS. The results showed that DHA and EPA inhibited LPS-induced MIF secretion, but these two n-3 PUFAs had no effect on the mRNA and protein levels of MIF. Immunoprecipitation analysis showed that LPS induced the interaction between MIF and ABCA1 which participates in MIF secretion pathway, and pretreatment of DHA and EPA suppressed the interaction. Furthermore, DHA and EPA repressed the colocalization of MIF and ABCA1 induced by LPS. SQ 22536, an inhibitor of protein kinase A (PKA), reversed the LPS-induced MIF secretion. Moreover, the interaction of MIF and ABCA1 was reduced in THP-1 macrophages pretreated with the PKA inhibitor in immunoprecipitation experiment. Thus, we suggest that LPS stimulates MIF secretion via activation of PKA signaling pathway. In conclusion, Our data reveal that DHA and EPA may inhibit LPS-induced MIF secretion by modulating the molecules involved in MIF secretion pathway and supply a novel insight to the mechanisms of n-3 PUFAs on anti-inflammation.
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Nguyen, Tuyet Mai [Verfasser]. "Elucidation of thiol protein oxidoreductase activity of the cytokine macrophage migration inhibitory factor (MIF) by biochemical redox and site specific mutagenesis analysis / vorgelegt von Nguyen Tuyet Mai". 2003. http://d-nb.info/967671175/34.
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Goupil, Mathieu. "Analyse de la réponse macrophagique au Candida albicans chez la souris transgénique exprimant le génome du VIH-1". Thèse, 2009. http://hdl.handle.net/1866/4045.
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La candidose oro-pharyngée (COP) est l’infection opportuniste la plus répandue chez les patients infectés au VIH-1. Un modèle de COP chez la souris transgénique (Tg) exprimant une partie du génome du VIH-1 (CD4C/HIVMutA) est maintenant disponible. Grâce à ce modèle, il est possible d’étudier les perturbations quantitatives et fonctionnelles des macrophages exprimant les gènes nef, rev et env du VIH-1 dans le contexte d’une COP. Cette étude démontre que la présence du transgène n’influence pas le pourcentage des macrophages dans la muqueuse buccale et le petit intestin, malgré le fait que la charge buccale de C. albicans soit significativement plus élevée chez les souris Tg. Cependant, l’expression du transgène cause une diminution de la production de H2O2 par les macrophages, ainsi que l’augmentation de la production de la cytokine proinflammatoire IL-6 et de la chimiokine MCP-1.Oro-pharyngeal candidiasis (OPC) is the most common opportunistic infection in HIV-1 infected patients. An OPC model using transgenic mice (CD4C/HIVMutA) expressing selected genes of the HIV-1 genome is now available. Using this model, it is now possible to study potential quantitative and functional disturbances in macrophages expressing the nef, rev and env genes of HIV-1 in the context of OPC. This study shows that transgene expression does not affect quantitative percentage values of macrophages in the oral mucosa and the small intestine, although burdens of C. albicans loads are increased in Tg mice. Transgene expression does induce diminished H2O2 production in macrophages, while increasing production of the proinflammatory cytokine IL-6 and the chemokine MCP-1.
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Σταθάς, Θεόδωρος. "Μελέτη του ρυθμιστικού ρόλου του παράγοντα αναστολής της μετανάστευσης των μακροφάγων (MIF) στην επίδραση των κορτικοειδών στην παραγωγή μεταλλοπρωτεασών και των ενδογενών αναστολέων τους, κυτταροκινών και κολλαγόνου στο ρινικό πολύποδα". Thesis, 2012. http://hdl.handle.net/10889/6152.
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Στην παρούσα διατριβή μελετήθηκε η έκφραση του παράγοντα αναστολής της μετανάστευσης των μακροφάγων (MIF) στον ιστό από ρινικό πολύποδα αλλά και στον φυσιολογικό ρινικό βλεννογόνο, καθώς και η ικανότητα αυτού να εξουδετερώνει την ανασταλτική δράση των γλυκοκορτικοειδών (ΓΚ) στην επαγόμενη από διάφορους αυξητικούς παράγοντες παραγωγή διαμεσολαβητών, όπως η IL-6 η MMP-1, η MMP-3 το κολλαγόνο τύπου-Ι και ο TIMP-1, που εμπλέκονται στη παθογένεια του ρινικού πολύποδα (ΡΠ). Ο MIF ανιχνεύθηκε στο μέσο καλλιέργειας όλων των ιστών και σε όλα τα εκχυλίσματα. Η έκφρασή του ήταν αυξημένη στον ρινικό πολύποδα σε σχέση με τον φυσιολογικό ρινικό βλεννογόνο. O TGF-β1 προκάλεσε δοσο- και χρονο-εξαρτώμενη αύξηση των επιπέδων της IL-6 του TIMP-1 και του κολλαγόνου τύπου-Ι, και παράλληλα ο TNF-α προκάλεσε δοσο- αλλά και χρονο-εξαρτώμενη διέγερση στην παραγωγή της IL-6 του TIMP-1 και των μεταλλοπρωτεασών MMP-1 και MMP-3. Η δεξαμεθαζόνη προκάλεσε στατιστικά σημαντική και δοσοεξαρτώμενη μείωση της επαγόμενης από τον TGF-β1 και TNF-α, παραγωγής της IL-6 του TIMP-1 του κολλαγόνου τύπου-Ι και των μεταλλοπρωτεασών MMP-1 και MMP-3. Διερευνώντας τον μηχανισμό μέσω του οποίου η δεξαμεθαζόνη ασκεί την κατασταλτική της δράση στην επαγόμενη τόσο από τον TGF-β1 όσο και από τον TNF-α, παραγωγή της IL-6, φάνηκε πως αυτή εκδηλώνεται κυρίως μέσω της επαγωγής αλλά και της προστασίας της ΜΚΡ-1 και κατά συνέπεια της καταστολής του μονοπατιού των ΜΑΡΚ και της ενεργοποίησης του ΑΡ-1, και λιγότερο μέσω της καταστολής της ενεργοποίησης του NF-κB. Ο ISO-1, ένας αναστολέας της δράσης του MIF, ενίσχυσε σημαντικά την κατασταλτική επίδραση της δεξαμεθαζόνης στα επίπεδα της IL-6 και του TIMP-1 στο μέσο καλλιέργειας ιστού από ΡΠ, ενώ αντίθετα προκάλεσε αναστροφή της κατασταλτικής δράσης της δεξαμεθαζόνης, η οποία ήταν στατιστικά σημαντική για την ΜΜΡ-1 όχι όμως και για την ΜΜΡ-3. Η ενίσχυση της κατασταλτικής δράσης της δεξαμεθαζόνης παρουσία του ISO-1, που κυμάνθηκε από 15.0% έως 20.5% θα πρέπει μάλλον να οφείλεται στην αναστολή του ενδογενούς MIF από τον ISO-1. Συμπερασματικά, η παρουσία του MIF στον ιστό του ρινικού πολύποδα, φαίνεται να εξασθενίζει το κατασταλτικό αποτέλεσμα της δεξαμεθαζόνης στην παραγωγή IL-6 και TIMP-1 από αυτόν τον ιστό, ενώ η ταυτόχρονη χρήση του αναστολέα του MIF, ISO-1 οδηγεί σε μια περαιτέρω ενίσχυση της κατασταλτικής δράσης της δεξαμεθαζόνης. Έτσι, είναι λογικό κατ΄αρχήν, να προταθεί πως η δημιουργία ενός φαρμακευτικού σχήματος που περιέχει κορτιζόλη και ένα αναστολέα του MIF, θα μπορούσε να είναι πιο αποτελεσματικό στην θεραπεία της ΡΠ. Απαιτούνται περαιτέρω πειράματα με συνδυασμό ΓΚ και αναστολέων του MIF για να μελετηθεί η επίδρασή τους στη παραγωγή και άλλων παραγόντων που εμπλέκονται στη παθογένεια της ΡΠ προκειμένου να εξαχθούν ασφαλέστερα συμπεράσματα.In the present study we investigated the expression of macrophage migration inhibitory factor (MIF) in nasal polyp tissues and also in normal nasal mucosa. The ability of MIF to neutralize the inhibitory effect of glucocorticoids on various growth factors induced expression of IL-6, TIMP-1, collagen type-I and matrix metalloproteinases MMP-1 and MMP-3, involved in the pathogenesis of nasal polyps, was studied. MIF was detected in all polyp tissue extracts and tissue culture conditioned media and its expression was increased in nasal polyps compared with normal nasal mucosa. TGF-b1 caused a dose-and time-dependent increase in levels of IL-6 of TIMP-1 and collagen type-I, while the TNF-a induced a dose-and time-dependent stimulation in the production of IL-6 of TIMP-1 and metalloproteinases MMP-1 and MMP-3. Dexamethasone caused a statistically significant and dose-dependent reduction induced by TGF-b1 and TNF-a, production of IL-6 of TIMP-1 of collagen type-I and the metalloproteinases MMP-1 and MMP-3. Investigating the mechanism by which dexamethasone exercises the suppressive action on both induced by TGF-b1 and by TNF-a, production of IL-6, showed that this occurs mainly through the induction and protection of MKP-1 and hence the suppression of the MAPK pathway and activation of AP-1, and less through the suppression of the activation of NF-kB. The ISO-1, an inhibitor of the action of MIF, significantly enhanced the suppressive effect of dexamethasone on the levels of IL-6 and TIMP-1 in tissue culture medium from nasal polyps. In contrary, ISO-1 induced inversion of the suppresive action of dexamethasone, which was statistically significant for MMP-1 but not for MMP-3. Enhancing of the suppresive action of dexamethasone in the presence of ISO-1, which ranged from 15.0% to 20.5% would probably be due to inhibition of endogenous MIF by ISO-1. In conclusion, the presence of MIF in nasal polyp tissue, appears to attenuate the suppressor effect of dexamethasone on the production of IL-6 and TIMP-1by this tissue, while simultaneously using the inhibitor of MIF, ISO-1 leads to an enhancement of dexamethasone activity. Therefore, it is reasonable to propose that the creation of a pharmaceutical regimen containing cortisol and an inhibitor of MIF, might be more effective in the treatment of nasal polyposis. Of course, requires further experiments with a combination of glucocorticoids and MIF inhibitors to study their effect on production of other factors involved in the pathogenesis of nasal polyposis in order to draw safer conclusions.