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Dissertations / Theses on the topic 'Interleukin-6'

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Published: 4 June 2021

Last updated: 1 July 2024

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1

Schebesta, Kathrin [Verfasser]. "Das Endothel sezerniert Interleukin-6 (IL-6) und stimuliert die adrenale Interleukin-6 und Aldosteronsynthese über einen Interleukin-6 unabhängigen Mechanismus / Kathrin Schebesta." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2015. http://d-nb.info/1079652612/34.

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2

OBAFEMI, TOLULOPE FESAYO. "THE EFFECTS OF INTERLEUKIN 6 AND INTERLEUKIN 10 ON FRAILTY IN C57BL/6 MICE." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/613394.

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Studies have shown that pro-inflammatory IL-6 and anti-inflammatory IL-10 interleukins may correlate to frailty and aging. This frailty can be defined in the context of clinical symptoms which include sarcopenia and osteoporosis, decreased activity level; or in the context of increased susceptibility to adverse health outcomes from a deficient immune system. In this experiment we tested a cohort of conditionally regulated IL-6 and IL-10 mice with controls (IL-6tg+.rtTA(r/r) (n=8), IL-10(-/-). IL-10tg+ rtTA(r/r) (n=10) and rtTA(r/r) (n=5)) under frailty assessments and immunological cell analysis. We were unable to successfully induce expression in the conditionally regulated mice. Subsequently, there was no difference in the frailty scores, weight, or temperature fluctuation between all three genotypes. As a preliminary study, there arose essential learning points of improvement that can be applied to future experiments concerning frailty in transgenic mice.

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3

Terry, Catherine. "Genetic control of Interleukin-6 gene." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342452.

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4

Höschen-Lihs, Jutta. "Interleukin-6- und Interleukin-2-Rezeptor als Aktivitätsmarker bei infektiöser Endokarditis." [S.l.] : [s.n.], 2005. http://archiv.ub.uni-marburg.de/diss/z2005/0327/.

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5

Siegmund, Annette. "Interleukin-11 - analog zu Interleukin-6 - ein direkter Modulator der Nebennierenrinde." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-83542.

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6

Desallais, Lucille. "Immunisation active à base de peptides, dérivés de l’IL-6 et de l’IL-1β, dans les maladies inflammatoires chroniques." Thesis, Paris, CNAM, 2013. http://www.theses.fr/2013CNAM0867.

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Les anticorps monoclonaux anti-cytokine ont constitué une révolution dans le traitement des maladies inflammatoires chroniques, mais leur utilisation présente des inconvénients (non réponse, résistance, effets secondaires, coûts élevés).Notre équipe développe une stratégie alternative originale, l’immunisation active à base de peptides de cytokines. Elle a pour but de faire synthétiser, par l’organisme même du patient, des anticorps neutralisant les effets pathogènes dus à l’excès de cytokines.Durant ma thèse, j’ai montré que l’immunisation active contre un peptide dérivé de l’IL-6 murine est protectrice dans un modèle murin de sclérodermie systémique. L’immunisation de singes avec l’équivalent humain entraîne une réduction significative des réactions inflammatoires locales suite à l’induction d’une réaction d’HSR. De plus, l’immunisation active contre deux peptides dérivés de l’IL-1β et de l’IL-23 conduit à la réduction de la sévérité de l’EAE.Ces résultats confortent l’intérêt de cibler les cytokines par l’approche d’immunisation active à base de peptides, qui pourra permettre de diversifier l’offre thérapeutique actuellement disponible
Monoclonal antibodies have been a revolution for the treatment of chronic inflammatory diseases, but their use shows major drawbacks (non-response, resistance, side effects and prohibitive costs).Our team develops an original alternative strategy: anti-cytokine peptide-based active immunization.The aim of the approach is to make the patient’s own organism produce antibodies capable of neutralizing the pathogenic effects of cytokine overproduction.During my PhD, I have demonstrated that active immunization against an IL-6 murine peptide confers clinical protection in a murine model of systemic sclerosis. Monkeys immunized against the human peptide also showed a significant decrease of local inflammatory reactions following a delayed-type hypersensitivity reaction. Moreover, active immunization against an IL-1β and an IL-23 murinepeptide led to a reduction of the severity of the EAE in mice.These results comfort the interest of anti-cytokine peptide-based active immunization, which should eventually widen the choice of therapeutics available for the patients

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7

Walter, Claudia. "Bestimmung der Zytokine Interleukin-1ra, Interleukin-6, Interleukin-10 und Interleukin-12 im Vaginalsekret bei Frauen mit Bakterieller Vaginose." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-28461.

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8

Slawik, Helen Christina. "Kontinuierliche Überexpression von Interleukin-6 im Zentralnervensystem lokale Applikation des Designerzytokins Hyper-Interleukin-6 im adulten Organismus der Ratte und Auswirkungen von exzitatorischen Neurotoxinen im Interleukin-6-transgenen Mausmodell /." [S.l.] : [s.n.], 2003. http://www.freidok.uni-freiburg.de/volltexte/842.

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9

Gopinathan, Ganga. "The effects of interleukin-6 on angiogenesis." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8186.

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Elevated levels of the inflammatory cytokine interleukin-6, IL-6, have been linked with poor prognosis in ovarian cancer patients by influencing tumour growth, invasion, angiogenesis and chemo-resistance. A clinical trial conducted in parallel with pre-clinical studies showed an anti-IL-6 antibody to have some activity in ovarian cancer patients and in xenograft models, via reduction in pro-inflammatory and angiogenic factors such as TNF-α, IL-8 and VEGF. Anti-IL-6 treatment also showed significant reductions in vascular area with decreased expression of an angiogenic factor Jagged1. The aim of my study was to investigate the effects of IL-6 on normal and tumour angiogenesis. I found that recombinant IL-6 stimulates angiogenesis in mouse and rat aortic ring assays and that it can also stimulate growth and migration of endothelial cells in vitro. IL-6 has similar potency as VEGF in inducing vessel sprouting. IL-6 itself does not induce VEGF in the endothelial cells I tested. Investigation of the effects of IL-6 on vessel maturation revealed a significant reduction in pericyte coverage of vessels treated with IL-6 compared with VEGF. Collectively, these data led to my hypothesis that ‘IL-6 drives aberrant angiogenesis, independent of VEGF signalling’. Investigating the mechanism by which IL-6 drives angiogenesis and leads to defective pericyte formation, I showed a link between IL-6 and the Notch ligands, Jagged1 and DLL4. My data suggested that IL-6 could stimulate Jagged1 in endothelial cells, whereas VEGF induces DLL4, the Notch ligand known to be involved in inducing stalk phenotype. Exploring previous findings to get a better understanding of the interaction of Notch ligands and pericyte recruitment also suggested a role of Angiopoeitin-2 in relation to IL-6 signalling. These observations were extended in IGROV-1 ovarian cancer xenografts treated with an anti-IL-6 antibody and by analysis of gene expression datasets from ovarian cancer biopsies. My results suggest therapeutic potential of combining inhibitors of IL-6 and VEGF in ovarian cancer.

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10

Sonnenberg, Sabine. "Tissue specific genetic regulation of Interleukin 6." Thesis, University of Southampton, 2009. https://eprints.soton.ac.uk/72590/.

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Interleukin 6 (IL6) is associated with arterial disease development, progression and surgical outcome. Raised levels of IL6 may play a causal role in disease development or may be the effect of pathology. An IL6 single nucleotide polymorphism (SNP) G- 174C has been identified and reported to associate with IL6 expression. However, conflicting results have emerged and both the relationship between IL6 and vascular disease and the precise effect of SNP G-174C in vivo in humans remains obscure. The aim of this study was to establish the effect of SNP G-174C in humans, in vivo in different tissues. Varicose vein surgery patients donated adipose tissue, skeletal muscle, vein and blood samples. Patients were genotyped for SNP G-174C. A new pre-mRNA assay was developed, using gel electrophoresis, restriction digest and fluorescence quantification, to measure the ratio of heterozygous allelic pre-mRNA transcription. IL6 mRNA expression in different tissues was also measured using relative real time PCR (RT-PCR) to assess effect of tissue type on expression profiles. mRNA expression within tissues was compared between G-174C genotypes, to further quantifying the association of SNP G-174C with transcript levels. The pre-mRNA assay showed higher expression for the C-allele, though not statistically significant. The pre-mRNA assay needed to detect low levels of intron retaining allelic pre-mRNA isoforms. Replicates and controls for residual genomic DNA were used to monitor assay precision. Adipose tissue gave the greatest precision in the pre-mRNA assay. In the RT PCR assay adipose tissue expressed significantly more IL6 mRNA than all other tissues examined. In vein and leukocytes subjects with the CC genotype expressed significantly higher levels of IL6 mRNA than subjects with GC or GG genotypes. There was a trend towards higher expression for the CC genotype in all tissue types. A significant though weak correlation between IL6 mRNA expression and age was demonstrated for vein and leukocytes. Adipose tissue may be an important source of IL6 compared to other tissues. This may be relevant for obesity associated diseases. Subjects with G-174C genotype CC showed a trend towards higher IL6 RNA expression. Further studies are necessary to clarify the effect of genotype on IL6 expression.

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11

McIlmoil, Stephen. "Regulation of adrenal steroidogenesis by interleukin-6 /." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd1976.pdf.

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12

McIlmoil, Stephen A. "Regulation of Adrenal Steroidogenesis by Interleukin-6." BYU ScholarsArchive, 2007. https://scholarsarchive.byu.edu/etd/975.

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Cortisol and dehydroepiandrosterone (DHEA) are steroids produced by the zona fasciculata (ZF) and reticularis (ZR), respectively, of the adrenal cortex. Both steroids are upregulated in response to adrenocorticotropic hormone (ACTH). Cortisol is a glucorticoid that is important in the regulation of inflammation and metabolism. DHEA is an adrenal androgen important in fetal growth and puberty but tends to decrease gradually after puberty in both men and women. DHEA has various effects on metabolism and immune function including inhibiting the effects of cortisol on some tissues. During the acute phase of stress, cortisol and DHEA rise due to an increase in ACTH released from the anterior pituitary. In contrast, during chronic stress, cortisol remains elevated but DHEA and ACTH levels decrease. Likewise, stress causes serum levels of IL-6 to increase. IL-6 increases cortisol release from the human and bovine adrenal cortex. IL-6 also decreases DHEA release from zona reticularis of the bovine adrenal gland. In humans the effect of IL-6 on DHEA production is still uncertain. To determine a possible mechanism of IL-6 on the zona fasciculata and reticularis, human H294R cells and bovine adrenal tissue were incubated in serum free medium containing IL-6, at various concentrations and incubation intervals. At the end of the incubation interval, mRNA or protein was extracted from the cells or tissue. Standard PCR, real time PCR, and western blot assays were used to determine the effects of IL-6 on the enzymes involved in cortisol and DHEA synthesis, steroidogenic factor-1 (SF-1), steroidogenic acute regulatory protein (StAR), and dosage sensitive sex reversal adrenal hypoplasia congenita critical region on the X chromosome, gene 1 (DAX-1). In human H295R cells and bovine zona fasciculata cells IL-6 caused an increase in SF-1, StAR, P450scc, 17α hydroxylase, 3β-hydroxysteroid dehydrogenase type 2 (3β HSD2), 21 hydroxylase, and 11β hydroxylase mRNA and protein. IL-6 caused DAX-1 mRNA and protein to decrease. These effects were manifest in a time dependent manner. Dose response treatments incubated for 60 min increased SF-1, StAR, P450scc, 17α hydroxylase, 3β HSD2, 21 hydroxylase, and 11β hydroxylase but there was not significant change between the different treatments of IL-6. The bovine zona reticularis stimulated with IL-6 showed a decrease in SF-1, StAR, P450scc, 17α hydroxylase, and 3β HSD2 with an increase in DAX-1 mRNA and protein. This response was manifest in a time dependent manner for both mRNA and protein, and the effect was dose-dependent for mRNA but not protein levels within the 60 min time period. These data provide a mechanism by which increased stress, physical or emotional, which increases IL-6 serum level, could increase cortisol and decrease DHEA. This would account for decreased immune function, increased blood pressure, and changes in metabolism.

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13

Benrick, Anna. "Cytokines in metabolic functions /." Göteborg : Section of Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, 2008. http://hdl.handle.net/2077/9608.

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14

Poe, Shaunta D. "Autocrine Effects of Catecholamines on Macrophage Release of Interleukin-6 (IL-6)." VCU Scholars Compass, 2006. http://hdl.handle.net/10156/1786.

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15

Leppert, Kyle McDonald McMurray Robert G. "The effect of glycogen depletion on responses of interleukin-1beta, interleukin-6, and interleukin-10 to maximal exercise." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2599.

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Thesis (M.A.)--University of North Carolina at Chapel Hill, 2009.
Title from electronic title page (viewed Oct. 5, 2009). "... in partial fulfillment of the requirement 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.

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16

Rau, Stefanie Maria. "Sepsis beim Hund: Interleukin-6 als prognostischer Parameter." Diss., [S.l.] : [s.n.], 2007. http://edoc.ub.uni-muenchen.de/archive/00007442.

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17

Wong, Pui-man Molly. "Hoxb3 mutation leads to interleukin-6 dependent plasmacytoma." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B3753564X.

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18

Wong, Pui-man Molly, and 黃佩文. "Hoxb3 mutation leads to interleukin-6 dependent plasmacytoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38695327.

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19

Bailey, Louise Lyn. "The development of Interleukin-6 specific peptide antagonists." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299390.

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20

Gineste, Aurélie. "Fer et immunité innée : vers une meilleure compréhension des mécanismes développés par l'hôte pour réduire le fer accessible aux pathogènes." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30117/document.

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Le fer est un élément essentiel à de nombreux processus physiologiques fondamentaux. Lors d'une infection, une forte compétition entre l'hôte et l'agent pathogène a lieu ; alors que la bactérie a besoin d'acquérir le fer de l'hôte, pour son développement et sa virulence, l'hôte déploie de nombreux mécanismes pour protéger ses stocks de fer. Il sécrète notamment un peptide capable de moduler l'homéostasie du fer au niveau systémique, l'hepcidine, qui va causer une diminution de la quantité de fer sérique, une rétention intracellulaire du fer et donc une restriction du fer accessible aux pathogènes. Lors d'une inflammation, l'expression de l'hepcidine est décrite dans la littérature pour être principalement induite via l'activation de deux voies de signalisation : la voie STAT3 et la voie BMP/SMAD, l'altération de chacune de ces voies conduisant à un défaut d'induction d'hepcidine. Cependant, nos précédentes observations publiées ont infirmé le rôle de l'IL6, ligand de la voie STAT3, dans la régulation de l'hepcidine en réponse au LPS, et ont suggéré l'implication d'un peptide appartenant à la famille du TGFb, l'activine B, dans la régulation de l'hepcidine via l'activation de la voie BMP/SMAD in vivo. Dans cette étude, nous nous sommes intéressés au rôle de l'activine B dans la régulation de l'hepcidine in vivo, lors d'une infection. Grâce à l'utilisation de souris invalidées pour le gène codant l'activine B (Inhbb-/-), nous avons confirmé que l'activine B était un ligand endogène de la voie BMP/SMAD dans le foie, puisqu'elle induit la phosphorylation des effecteurs SMAD en réponse au LPS. Cependant, nous avons pu clairement démontrer que l'activine B, et donc l'augmentation de la phosphorylation des effecteurs SMAD, ne participaient pas à la régulation de l'hepcidine in vivo, en réponse à l'infection. Nous nous sommes alors intéressés à l'implication de l'IL6 dans la régulation de l'hepcidine. Alors que l'absence d'Il6 n'altère pas l'induction de l'hepcidine in vivo en réponse au LPS, cette cytokine semble jouer un rôle clé pour la réponse de l'hôte lors d'une infection par une bactérie. Dans ce contexte, la littérature décrit l'importance de l'IL6 pour une réponse immunitaire protectrice de l'hôte lors d'une infection. Lors d'une infection, nous proposons donc l'implication d'une nouvelle voie de signalisation dans l'expression de l'hepcidine. De plus, nous suggérons un rôle important de l'IL6, non pas dans la régulation transcriptionnelle de l'hepcidine, mais pour la protection de l'hôte lors d'une infection bactérienne. Enfin, nos résultats montrent qu'un niveau d'activation basal de la voie BMP/SMAD est requis pour une induction d'hepcidine lors d'inflammation, et que l'augmentation de la phosphorylation des effecteurs SMAD observée en réponse à l'inflammation ne participe pas à cette régulation
Iron is essential for several fundamental metabolic processes. During infection, a strong competition between the host and the pathogen occurs; while the bacteria needs to acquire iron from the host, for its growth and virulence, hosts have developed several mechanisms to protect its iron stores. In particular, the host produces a peptide in order to modulate systemic iron homeostasis, hepcidin. Hepcidin decreases the amount of circulating iron, causes intracellular iron retention and thus a restriction of accessible iron to pathogens. During inflammation, hepcidin expression is described in the literature to be mainly mediated through activation of two signaling pathways: the STAT3 and the BMP/SMAD pathways. Impairment of one of these pathways leads to an impaired hepcidin induction. However, our previous published observations did not support the role of IL6, the major ligand of STAT3 pathway, in the regulation of hepcidin in response to LPS, but suggested the involvement of another protein, that belongs to the TGFb family, activin B, in the regulation of hepcidin via the activation of the BMP/SMAD pathway in vivo. In this study, we investigated the role of activin B in the regulation of hepcidin in vivo, during infection. By using knockout mice for the gene encoding activin B (Inhbb-/-), our results suggest that activin B is not involved in the regulation of hepcidin in vivo in response to infection. We then investigated the function of IL6 in the regulation of hepcidin. Although the absence of IL6 does not affect the induction of hepcidin in vivo in response to LPS, this cytokine appears to play a key role in the host response during bacterial infection. Indeed, the literature describes the importance of IL6 for a protective immune response of the host during infection. During infection, we hypothesize that another signaling pathway regulates hepcidin expression. In addition, we suggest an important role of IL6, not in the transcriptional regulation of hepcidin, but for the host protection during a bacterial infection. Finally, our results also show that basal level of BMP/SMAD pathway is required for an appropriate induction of hepcidin during inflammation

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21

Woolley, Jane Alison. "The production, assessment and application of antibodies to human interleukin-6 (IL-6)." Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338809.

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22

Schmid, Birgit. "Regulation of the human oxytocin receptor gene by interleukin-1ß and interleukin-6 in vitro." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0012/MQ59875.pdf.

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23

Björnstedt, Bennermo Marie. "On the genetic variation of interleukin-6 in health and coronary heart disesase /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-253-5/.

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24

Azbil, Tatiana. "Nachweis von Candida-Spezies und Bestimmung der Zytokine Interleukin-1 beta, Interleukin-1ra, Interleukin-4, Interleukin-6, Interleukin-8, Interleukin-10 und Interleukin-12 im Vaginalsekret und im Serum bei Schwangeren in Relation zum Gestationsalter." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-57576.

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25

Harré, Eva-Maria. "Die Rolle von Interleukin-6 (IL-6) in der zentralnervös vermittelten Fieberentstehung der Ratte." Wettenberg : VVB Laufersweiler, 2003. http://deposit.d-nb.de/cgi-bin/dokserv?idn=968960545.

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26

Hamzic, Namik. "The Role of Interleukin-6 in the Febrile Response." Doctoral thesis, Linköpings universitet, Cellbiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-87453.

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Everyone who has been exposed to influenza or a bacterial infection knows how it feels to be sick. Apart from not being willing to participate in social activities, losing your appetite and experiencing pain, you have also most likely suffered from increased body temperature which defines fever, one of the most prominent signs of an acute ongoing infection. Invading the body, the infectious microorganisms are combated by the activated innate and adaptive immune systems, and the impaired balance is thus restored. While fever is an event that is controlled by the central nervous system, it has for long been debated how the inflammatory signals generated in the periphery communicate with the brain that is protected by the bloodbrain barrier which prevents large molecules such as cytokines from entering into the brain parenchyma. Previous studies from our group have provided evidence in support of the existence of a pathway across the blood-brain barrier by demonstrating that proinflammatory cytokine interleukin-1 transfers the inflammatory message to the brain through binding to its receptors situated in the brain vessels. This will subsequently trigger the production of the prostaglandin E2 (PGE2) that enters the brain and exerts its effect by binding to the receptors located on the thermoregulatory neurons. Interleukin-6 (IL-6) is another cytokine essential for fever signaling; however, the mechanism has not yet been identified. The research on which this thesis is based aimed at elucidating the role of IL-6 in inflammatory induced fever. In paper I, we demonstrated that mice incapable of producing inflammatory PGE2 still responded with an intact cytokine production in the brain upon peripheral lipopolysaccharide (LPS) stimulation. Thus, although the mice had induced expression of inflammatory cytokines in the brain, this was not sufficient for a fever response without simultaneous production of PGE2. The relationship between IL-6 and PGE2, both essential for fever, was further investigated in paper II, focusing on clarifying the mechanism by which IL-6 controls fever. We demonstrated that mice deficient in IL-6 did not respond with fever upon peripheral LPS administration despite an intact expression of PGE2 in the brain. In contrast, upon intracerebroventricular administration of PGE2 into the brain, a dose-dependent fever response was monitored in IL-6 deficient mice. Thus, we suggest that IL-6 exerts its effect neither up- nor downstream from PGE2, and propose instead that IL-6 may act alongside the PGE2 and regulate the process that deals with the transport of and binding of PGE2 onto its receptors. To further investigate the elusive role of IL-6 in fever, we performed a microarray analysis to identify the genes that were differentially expressed in the brain of LPS-challenged IL-6 deficient mice compared to wild type mice (paper III). We demonstrated that mice lacking IL-6 displayed two-times lower expression of lipocalin-2 in the hypothalamus. IL-6 and lipocalin-2 were directly related to each other since peripherally administrated IL-6 induced the expression of lipocalin-2 in cells associated with the brain vessels. Lipocalin-2 induced by LPS was expressed by brain endothelial cells and partly co-localized with cyclooxygenase-2, one of the enzymes essential for inflammatory PGE2 production in the endothelial cells. We also demonstrated that lipocalin-2 in a sex-dependent and ambient temperature-specific manner may be implicated in thermogenesis. We have thus identified a new factor in the IL-6 regulated fever pathway, but the pathway is still not understood. On important question that remained to be answered was in which compartment IL-6 was needed for the signaling. This question was studied further in paper IV, where we investigated the role of hematopoietically produced IL-6 in fever by constructing chimeric mice. We concluded that IL-6 produced by cells of non-hematopoietic origin is critical for the LPSinduced fever while hematopoietically produced IL-6 plays only a minor role in contributing to fever.

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27

Bußmeyer, Ingo [Verfasser]. "Struktur und Funktion von viralem Interleukin-6 / Ingo Bußmeyer." Kiel : Universitätsbibliothek Kiel, 2008. http://d-nb.info/1019669802/34.

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28

Voyle, Roger Bruce. "Mechanisms of intracellular and extracellular cytokine production from the human leukaemia inhibitory factor gene." Title page, contents and summary only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phv975.pdf.

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Addendum attached to back facing leaves. Includes bibliographical references (leaves 172-199). The findings establish leukemia inhibitory factor, and possibly oncostatin M, as new members of a small but growing class of cytokines produced in an intracellularly active form and also suggest that the production of alternate transcripts and intercellularly-retained proteins may be a common and important feature of cytokines of the IL-6 and other families.

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29

Kampshoff, Jörg. "Die Wirkung der Interleukine 4, 10 und 13 auf die Koinkubation von Endothelzellen und mononukleären Zellen, gemessen an der Freisetzung von PDGF, Interleukin-1-[beta] [Interleukin-1-beta] und Interleukin-6." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972057684.

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30

Hu, Yuli. "Compounds that Inhibit Cytokine-Induced Interleukin-6 Expression in a Monocytic Cell Line." Ohio University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1420708103.

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31

Hauk, Thomas. "Einfluss von Makrophagen und IL-6 auf die axonale Regeneration bei der adulten Ratte." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-65621.

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32

Asbagh, Layka Abbasi Doymaz Fuat. "Investigating the role of zoledronic acid on interleukin-6 cytokine expression in prostate cancer cell lines/." [s.l.]: [s.n.], 2006. http://library.iyte.edu.tr/tezlerengelli/master/biyoteknoloji/T000552.pdf.

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33

Knuth, Berenice Scaletzky. "Prevalência de depressão e níveis séricos de IL-6, em pacientes em hemodiálise." Universidade Catolica de Pelotas, 2012. http://tede.ucpel.edu.br:8080/jspui/handle/tede/283.

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BACKGROUND: In hemodialysis patients, depression appears as the most common psychopathological condition. States of advanced chronic kidney disease and dialysis are associated with a state of chronic inflammation. Depression has been linked to activation of the immune system characterized by high levels of pro-inflammatory cytokines. In this study we investigated the possible correlations between depression, and interleukin-6 (IL-6) in hemodialysis patients. METHODS: Seventy-five hemodialysis patients were enrolled in a cross-sectional study from September to November of 2011 in Pelotas/RS. Demographic data was obtained from a questionnaire and the Beck Depression Inventory (BDI), used to determine the presence or absence of depression symptoms. Biochemical parameters, dialysis dosage delivery, and IL-6 serum levels were measured. RESULTS: Prevalence of depression among hemodialysis patients was 48% (BDI ≥ 14). In biochemical assessments, depressed patients showed a decrease in urea (p = 0.01) and increase of IL-6 (p = 0.04) levels. The correlation analysis between BDI scores and the biochemical variables showed that BDI was negative correlated with urea (p = 0.03) and potassium (p = 0.04), but not with IL-6 levels. CONCLUSION: Hemodialysis patients with depression showed higher levels of IL-6 but the severity of depressive symptom was not correlated with levels of this cytokine.
A insuficiência renal crônica (IRC) é definida como a perda progressiva e irreversível da função renal. Em sua fase mais avançada, (chamada de fase terminal da insuficiência renal crônica) na qual os rins não conseguem mais manter a normalidade do meio interno, é necessário realizar a substituição da função renal. Tal procedimento pode ser realizado através de hemodiálise, diálise peritoneal ou transplante renal8. Atualmente, no Brasil, mais de 70.000 pacientes são dependentes de terapia renal substitutiva, com gasto anual de cerca de R$ 2,0 bilhões. Com base no grande número de grupos de risco, a previsão é que esse número possa duplicar nos próximos 5 anos, ultrapassando os 125 mil casos em 201016. As causas mais comuns de IRC são: diabetes (42,9%), hipertensão, doença de grandes vasos (26,4%), glomerulonefrite (9,9%) entre outras causas5. Alexander Almeida e Alexandrina Meleiro, em 2000, descreveram que a depressão maior, apesar de provavelmente ser a desordem psiquiátrica mais comum nos pacientes com IRC, permanece largamente subdiagnosticada. Existem evidências de que a depressão diminui a aderência ao tratamento da IRC e influencie negativamente a qualidade de vida. Diante disto, revela-se um fator importante de risco para mortalidade cardiovascular, e aumente em até 15 vezes a taxa de suicídio, podendo ser um preditor independente de menor sobrevida1. Estudos de revisão da literatura citam que a prevalência de depressão em pacientes em diálise varia de 0 a 100%, sugerindo que a prevalência dessa doença nesta população é ainda incerta10. A depressão maior, de acordo com os critérios do DSM-IV, pode se apresentar através de: humor deprimido, perda de prazer ou interesse notavelmente diminuído nas atividades prazerosas, distúrbios do sono, alteração do apetite e peso, perda de energia, ideação suicida entre outros6. A depressão tem sido associada à ativação do sistema imunológico caracterizada por elevados níveis de citocinas proinflamatórias e proteínas positivas da fase aguda14. Alguns estudos demonstraram que os níveis de citocinas e TNF-α estão aumentados em pacientes com depressão14. As citocinas são um grupo de proteínas (polipeptídeos) responsáveis pelas mediações das conexões imunocerebrais e desempenham um papel importante na patogênese da depressão devido ao seu efeito nos neurotransmissores e neuro-hormonios15. Neste respeito à depressão maior, esta tem sido associada com o aumento continuado dos níveis de citocinas; inclusive, tem sido significativamente implicada no desenvolvimento das desordens psiquiátricas, principalmente na depressão maior 13. As citocinas e outras moléculas têm impacto nas funções neuropsiquiátricas como o humor e a cognição, através da modulação da anatomia e da função neuronal. A plasticidade neuronal é importante para a regulação do humor, cognição e comportamento durante toda a vida. As citocinas e outros fatores imunológicos desempenham um papel fundamental na modulação cerebral; entretanto, exposição crônica a citocinas proinflamatórias podem causar dano na plasticidade neuronal, contribuindo para desordens cognitivas e alteração de humor13. Assim, uma vez que entre pacientes com IRC há grande incidência de sintomas depressivos, os objetivos deste estudo consistem em determinar a prevalência de depressão dos pacientes com IRC, em um serviço de hemodiálise, na cidade de Pelotas e identificar os possíveis biomarcadores, como a IL-6, nos fatores causadores do desenvolvimento da depressão. Tais fenômenos podem ajudar a melhorar o reconhecimento e o monitoramento dessa patologia

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Kirschmer, Stefanie [Verfasser]. "Untersuchung der potentiellen Biomarker Picalm, Interleukin-1beta, Interleukin-6, Interleukin-8 und Tumor-Nekrose-Faktor alpha im Liquor von Alzheimerpatienten / Stefanie Kirschmer." Ulm : Universität Ulm. Medizinische Fakultät, 2014. http://d-nb.info/104956149X/34.

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Loung, Le Anh. "Genetic variations in the interleukin-6(IL-6) gene : implication in coronary heart disease (CHD)." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406589.

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O'Brien, John D. "The Effect of Small Organic Compounds on Triple Negative Breast Cancer Cells." Ohio University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1344436677.

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Wang, Chun-Wei. "Quantitative protein detection in serum samples using fiber-optic biosensors." Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008m/wang.pdf.

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Bradaric, Christian. "Interaktion coxsackieviraler Proteasen mit dem kardioprotektiven Interleukin-6-Typ-Signaltransduktionsweg." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=978987195.

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Kalai, Michaël. "Structure-function analysis of human interleukin-6 and its receptor." Doctoral thesis, Universite Libre de Bruxelles, 1996. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212341.

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Becker, Karin Beate [Verfasser]. "Das Interleukin 6-System bei Alzheimer Demenz / Karin Beate Becker." Bonn : Universitäts- und Landesbibliothek Bonn, 2012. http://d-nb.info/1043509836/34.

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Laumen, Susanne [Verfasser]. "Die Expression von Interleukin-6 während der Frakturheilung / Susanne Laumen." Ulm : Universität Ulm. Medizinische Fakultät, 2014. http://d-nb.info/1046890093/34.

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Riethmüller, Steffen [Verfasser]. "Die Entstehung des humanen löslichen Interleukin-6 Rezeptors / Steffen Riethmüller." Kiel : Universitätsbibliothek Kiel, 2016. http://d-nb.info/1118499859/34.

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Reddy, Bindu. "Interleukin-6 Levels in Generalized and Localized Aggressive Periodontitis Patients." VCU Scholars Compass, 2004. http://scholarscompass.vcu.edu/etd/1284.

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AbstractINTERLEUKIN-6 LEVELS IN GENERALIZED AND LOCALIZED AGGRESSIVE PERIODONTITIS PATIENTSBy Bindu Reddy, D.D.S.A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at the Virginia Commonwealth UniversityVirginia Commonwealth University, 2004Major Director: Joseph V. Califano, D.D.S., Ph.D.Associate Professor, Department of Periodontics Periodontitis is an inflammatory disease involving the supporting structures of the dentition. Many studies have shown that there is a relationship between periodontal disease, the presence of pro-inflammatory cytokines, and systemic disease such as cardiovascular disease and diabetes mellitus. The purpose of this study was to measure serum Interleukin-6 levels in generalized and localized aggressive periodontitis and non-periodontitis patients and look for relationships with measures of disease severity. We also examined variables known to have a relationship with IL-6. A total of 172 subjects, comprising three periodontal subgroups, non-periodontitis (NP=61), generalized aggressive periodontitis (GAP=77), and localized aggressive periodontitis (LAP= 34), had serum samples evaluated for IL-6 levels using a highly sensitive ELISA test. The IL-6 levels were compared with clinical and demographic data including age, race, gender, number of teeth, probing depth, attachment loss, bleeding index, plaque index, gingival index, cotinine levels, smoking status, and CRP levels. Using multiple regression analysis, smoking status (p=0.0015) was the only variable found to have a significant relationship with IL-6 levels for all three groups.

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Al-Tae, Firas. "Biology of interleukin-6 production by human natural killer cells." Thesis, University of Liverpool, 2012. http://livrepository.liverpool.ac.uk/8573/.

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NK cells secrete a variety of immune-regulatory cytokines and chemokines such as interferon - γ (IFN-γ) and tumour necrosis factor- α (TNF-α). However, in some of infections where NK cells have an important role in the defence mechanism, IL-6 appears to play a significant anti-viral role. Considering the role of both IL-6 and NK cells in these infections raises the possibility that IL-6 secretion by NK cells could be a main defence mechanism against them. Morover, NK cell-mediated IL-6 secretion may provide a critical link between the innate and adaptive immune response of the host. Furthermore, changes in this pathway in various autoimmune diseases, for example rheumatoid arthritis (RA) may be relevant for the pathogenesis of these disorders. The results presented in this thesis demonstrated that peripheral blood NK cells from healthy individuals have the ability to secrete IL-6 after co-culture with target cells against which these cells are known to exhibit direct cytotoxicity (either K562 or HeLa cells). The described secretory response was rapid, with IL-6 being significantly higher as early as 1 hour in HeLa co-cultures compared to 6 hours in case of K562 co-cultures. These findings were further confirmed when NK cells were activated alone with high doses of IL-2 or with non specific chemical activators (PMA+ ionomycin). These experiments clearly showed that NK cells have the potential to secrete IL-6 following activation. To analyse whether IL-6 secretion in the co-culture experiments was the result of direct cell-cell interactions between NK cells and the target cells or was induced by the presence of soluble mediators, co-culture experiments were set up where the target cells were separated from NK cells using a 0.4 µm pore size inserts. Separating NK cells and target cells abolished increases in cytokine production proving that direct interaction between NK cells and target cells is necessary for triggering IL-6 production by NK cells, as the semi-permeable membrane of Transwell chambers allows for the free passage of soluble factors but prevents direct cell-cell contact. Investigating the activating pathway which triggers the secretion of IL-6 by NK cells was the next step. This aim was achieved by inducing NK cell activation with immobilized antibodies against NK cell activating receptors and assessing the effect of the engagement of these receptors on peripheral blood NK IL-6 gene expression and protein secretion by quantitative real time PCR and ELISA.The results demonstrated that NKG2D and NKp46 were the two main receptors involved in the IL-6 mRNA expression and secretion by NK cells. The final aim of this thesis was to evaluate the biological significance of this secretion through an in vitro experimental model. We hypothesized that IL-6 secreted by NK cells could contribute to the migration of other inflammatory and immune cells to the site of inflammation. This hypothesis was based on the observations of others that IL-6 could induce direct CD4+ T cell migration. To test this hypothesis, an in vitro transmigration assay using Transwell inserts with 8 and 3 µm pore size were used. Our results demonstrated that CD4+ T cell migration in response to NK cells was inhibited by about 30% in the presence of neutralizing antibody to IL-6. These results signify the relative biological importance of IL-6 induced secretion by NK cells. In conclusion NK cells can contribute to IL-6 secretion. Given that NK cells appear at inflammation sites at the earliest stages of the process, where the number of other cells with a potential to secrete IL-6 is low, it is possible that NK cell-mediated IL-6 secretion is essential in orchestrating and potentiating the later stages of the adaptive immune response.

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Ravi, Arjun Kumar. "Macrophages, monocytes and interleukin-6 in chronic obstructive pulmonary disease." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/macrophages-monocytes-and-interleukin6-in-chronic-obstructive-pulmonary-disease(806db259-02de-4d50-8c2e-5b57cb2425c0).html.

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Background: COPD is associated with an increased lung macrophage burden. Whilst lung macrophages may self-renew, recruitment of peripheral blood monocytes from the systemic circulation is considered to represent their principal means of replenishment. Through modulating expression of monocytic chemokines CCL2/CCL3 and their respective receptors (CCR2/CCR1+CCR5), IL-6 could play a key role in facilitating the recruitment of monocytes to the lungs of COPD patients. COPD is associated with enhanced pulmonary and systemic IL-6 levels; concentrations of the soluble IL-6 receptor sIL-6R may be an important determinant of IL-6 signalling in COPD. Trans-signalling through sIL-6R, IL-6 may facilitate recruitment of monocytes in COPD by influencing chemokine and chemokine receptor expression. Aims: 1) To compare levels of IL-6, sIL-6R, CCL2 and CCL3 in the plasma and sputum of COPD and controls. 2) To examine of the effects of IL-6 stimulation on monocyte chemokine receptor gene expression (CCR1, CCR2 and CCR5). 3) To compare subtypes (CD14++CD16-, CD14+CD16+, CD14-CD16++) and chemokine receptor expression (CCR1, CCR2, CCR5) of monocytes in COPD (paired stable & exacerbating) and controls. 4) To compare the migratory ability of monocytes from COPD and controls. 5) To compare numbers of marginated CX3CR1+ monocytes in the pulmonary microvasculature and proliferation status (Ki67 positivity) of alveolar macrophages in COPD and controls. Methods: 1) MSD soluble marker analysis was performed on plasma and sputum supernatant. 2) Monocytes underwent stimulation with IL-6 and sIL-6R; chemokine receptor expression was determined by quantitative PCR. 3) Flow cytometry was performed on whole blood to determine monocyte subtype and chemokine receptor expression. 4) Monocyte migration towards sputum supernatant was assessed using a transwell system incorporating fluorescence based detection of DNA from migrated cells. 5) Immunofluorescence and immunohistochemistry was performed on lung tissue (obtained from patients undergoing surgical resection of lung carcinoma) to identify marginated (CX3CR1+CD14+, CX3CR1+CD16+) monocytes and proliferating alveolar macrophages (Ki67) respectively. Results and Conclusion: Levels of sIL-6R were increased in the lungs and systemic circulation of COPD patients implying potential for enhanced IL-6 trans-signalling: monocytes cultured in the presence of IL-6+sIL-6R upregulated expression of the CCR5 gene. A greater proportion of circulating COPD CD14++CD16- and CD14+CD16+ monocytes were demonstrated to express CCR5 compared to controls indicating that CCR5 ligands may have an important influence over monocyte migration in COPD. Levels of CCR5 ligand CCL3 were significantly elevated in COPD sputum supernatant; IL-6 levels were positively associated with CCL3 indicating that IL-6 trans-signalling may mediate lung chemokine expression. Nevertheless, COPD monocytes demonstrated impaired migration towards sputum supernatant and reduced margination to pulmonary microvessels. Despite this, the number of alveolar macrophages in COPD was increased; however this was not likely to be related to self-replication owing to low alveolar macrophage Ki67 expression.

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Wendland, Sylke [Verfasser]. "Interleukin-6-, Interleukin-10- und TNF-alpha-Plasmaspiegel bei Patienten mit transplantations-assoziierter lymphoproliferativer Erkrankung / Sylke Wendland." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1035406365/34.

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Nitz, Rebecca [Verfasser], and Jürgen [Gutachter] Scheller. "Unterschiede in der proteolytischen Spaltung von Interleukin-6- und Interleukin-11-Rezeptor / Rebecca Nitz ; Gutachter: Jürgen Scheller." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2016. http://d-nb.info/1121745717/34.

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Schlichting, Nadine. "Palmitat induzierte Expression von IL-6 und MCP-1 in humanen Detrusormyozyten vs. bakteriell induzierter Entzündungsreaktion - ein möglicher Zusammenhang zwischen diabetischen Stoffwechsel und Infektionen der Harnblase." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-67731.

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Adipöse Patienten und Typ-2-Diabetiker zeigen ein erhöhtes Risiko für Harnwegsinfekte. Die Ursache der höheren Prävalenz ist noch nicht nachhaltig geklärt. Bekannt ist, dass Typ-2-Diabetiker erhöhte Konzentrationen freier Fettsäuren im Blut aufweisen. Der veränderte Fettstoffwechsel könnte neben bakteriellen Ursachen ein möglicher Grund für abakterielle Entzündungsreaktionen der Harnblase sein. Zur Prüfung dieser Hypothese wurden zeit- und konzentrationsabhängig kultivierte humane Detrusormyozyten im Vergleich zur Lipopolysaccharid (LPS) induzierten Entzündungsreaktion mit Palmitat stimuliert. Es wurde geprüft, ob eine autokrine und/oder endokrine Regulation des IL-6-Signalwegs vorliegt. Im Fokus standen insbesondere die IL-6- und MCP-1-Expression und deren möglichen regulatorischen Proteine gp80, gp130, NF-κB, STAT3, SOCS3 und MEK1. Die Stimulationsversuche mit LPS und Palmitat zeigen einen differenten zeit- und konzentrationsabhängigen Effekt auf die IL-6- und MCP-1-Expression in den humanen Detrusormyozyten. LPS und Palmitat induzieren eine zeitabhängige autokrine Regulation der IL-6-Signalkaskade über phosphoryliertes STAT3 und Feedback-mechanismen via SOCS3. Sowohl LPS als auch Palmitat bewirken über 48h eine mögliche endokrine Regulation des IL-6-Signalwegs. Zusammenfassend zeigt die Palmitatstimulation zeit- und konzentrationsabhängig einen stärkeren Effekt auf die IL-6-Signalwirkung als die Stimulation mit LPS
Background: Urinary tract infections (UTI) are more frequent in type-2 diabetes mellitus patients than in subjects with normal glucose metabolism. The mechanisms underlying this higher prevalence of UTI are unknown. However, cytokine levels are altered in diabetic patients and may thus contribute to the development of UTI. Increased levels of free fatty acids (FFA), as observed in obese patients, can induce IL-6 production in various cell types. Therefore we studied the effects of the free fatty acid palmitate and bacterial lipopolysaccharide (LPS) on interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) expression and secretion in cultured human bladder smooth muscle cells (hBSMC). Methodology/Principal Findings: Biopsies were taken from patients undergoing cystectomy due to bladder cancer. Palmitate or LPS stimulated hBSMC were analysed for the production and secretion of the IL-6, gp80, gp80soluble, gp130, MCP-1, pSTAT3, SOCS3, NF-kB and SHP2 by quantitative PCR, ELISA, Western blotting, and confocal immunofluorescence. In signal transduction inhibition experiments we evaluated the involvement of NF-kB and MEK1 in IL-6 and MCP-1 regulation. Palmitate upregulates IL-6 mRNA expression and secretion via NF-kB dependent pathways in a concentration- and timedependent manner. MCP-1 was moderately upregulated by palmitate but was strongly upregulated by LPS involving NF-kB and MEK1 dependent pathways. Soluble IL-6 receptor (gp80soluble) was downregulated by palmitate and LPS, while membrane-bound gp80 was moderately upregulated. LPS increased SOCS3 and SHP2, whereas palmitate only induced SOCS3. Secondary finding: most of the IL-6 is secreted. Conclusions/Significance: Bacterial infection (LPS) or metabolic alterations (palmitate) have distinct effects on IL-6 expression in hBSMC, (i) short term LPS induced autocrine JAK/STAT signaling and (ii) long-term endocrine regulation of IL-6 by palmitate. Induction of IL-6 in human bladder smooth muscle cells by fatty acids may represent a pathogenetic factor underlying the higher frequency and persistence of urinary tract infections in patients with metabolic diseases

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Baran, Paul [Verfasser], Jürgen [Gutachter] Scheller, and Ulrich [Gutachter] Flögel. "Quantifizierung von Interleukin-6/löslichen Interleukin-6 Rezeptorkomplexen und Etablierung eines Nanopartikel-Zelltracking Systems über synthetische Cargo-Internalisierungsrezeptoren / Paul Baran ; Gutachter: Jürgen Scheller, Ulrich Flögel." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2018. http://d-nb.info/1163449873/34.

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Engelowski, Erika [Verfasser]. "Design synthetischer Zytokinrezeptoren für Interleukin-6- und Interleukin-23-artige Zytokine und Analyse der Rolle von Interleukin-23 in kardialer Ischämie / Erika Engelowski." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2019. http://d-nb.info/1188017705/34.

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