Gotowe bibliografie tematyczne / IL-6

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Gotowa bibliografia na temat „IL-6”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 maja 2024

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Artykuły w czasopismach na temat "IL-6"

Toshiro, Shimamura, Taki Shinsuke, Honda Hideo, Yokota Masataka, Ito Satoru i Takahara Yoshiyuki. "Analysis of interleukin 6 (IL-6)/IL-6 receptor system using monoclonal anti-IL-6 antibodies". Molecular Immunology 28, nr 11 (listopad 1991): 1155–61. http://dx.doi.org/10.1016/0161-5890(91)90001-z.

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TAMM, IGOR. "IL-6". Annals of the New York Academy of Sciences 557, nr 1 (28.06.2008): 478–89. http://dx.doi.org/10.1111/j.1749-6632.1989.tb24040.x.

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Gaillard, O. "Interleukine 6 (IL-6)". Immuno-analyse & Biologie Spécialisée 17, nr 3 (czerwiec 2002): 140–42. http://dx.doi.org/10.1016/s0923-2532(02)01191-2.

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Matsuda, Tadashi, i Toshio Hirano. "Interleukin 6 (IL-6)". Biotherapy 2, nr 4 (październik 1990): 363–73. http://dx.doi.org/10.1007/bf02170085.

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Hansen, MB, M. Svenson, M. Diamant, C. Ross i K. Bendtzen. "Interleukin-6 (IL-6) autoantibodies and blood IL-6 measurements [letter]". Blood 85, nr 4 (15.02.1995): 1145. http://dx.doi.org/10.1182/blood.v85.4.1145.bloodjournal8541145.

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Usha, Prof. "IL-4 and IL-6 in Bronchial Asthma Does IL-6 Plays More Important Role than IL-4? A Preliminary Study". Journal of Medical Science And clinical Research 05, nr 04 (18.04.2017): 20446–50. http://dx.doi.org/10.18535/jmscr/v5i4.115.

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Van Wagoner, Nicholas J., Jae-Wook Oh, Pavle Repovic i Etty N. Benveniste. "Interleukin-6 (IL-6) Production by Astrocytes: Autocrine Regulation by IL-6 and the Soluble IL-6 Receptor". Journal of Neuroscience 19, nr 13 (1.07.1999): 5236–44. http://dx.doi.org/10.1523/jneurosci.19-13-05236.1999.

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Baran, Paul, Rebecca Nitz, Joachim Grötzinger, Jürgen Scheller i Christoph Garbers. "Minimal Interleukin 6 (IL-6) Receptor Stalk Composition for IL-6 Receptor Shedding and IL-6 Classic Signaling". Journal of Biological Chemistry 288, nr 21 (5.04.2013): 14756–68. http://dx.doi.org/10.1074/jbc.m113.466169.

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Jostock, Thomas, Guido Blinn, Christoph Renné, Karl-Josef Kallen, Stefan Rose-John i Jürgen Müllberg. "Immunoadhesins of interleukin-6 and the IL-6/soluble IL-6R fusion protein hyper-IL-6". Journal of Immunological Methods 223, nr 2 (marzec 1999): 171–83. http://dx.doi.org/10.1016/s0022-1759(98)00218-x.

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Pooran, Nakechand, Anant Indaram, Pankaj Singh i Simmy Bank. "Cytokines (IL-6, IL-8, TNF)". Journal of Clinical Gastroenterology 37, nr 3 (wrzesień 2003): 263–66. http://dx.doi.org/10.1097/00004836-200309000-00013.

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Rozprawy doktorskie na temat "IL-6"

Terrades, Garcia Nekane. "Interleukin-6 (IL-6)/IL-6 receptor and persistence of inflammation in Giant Cell Arteritis. Effects of IL-6 receptor blockade with tocilizumab". Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/668038.

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Giant cell arteritis (GCA) is a chronic granulomatous vasculitis affecting large- and medium-sized vessels. This disease can lead to different symptoms related to vascular or systemic inflammation, such as fever and visual loss, and its exact etiology remains to be elucidated. Current treatment of GCA patients is based on glucocorticoids administration. However, not all patients respond properly to this treatment and the disadvantages associated to glucocorticoids promotes the search for new therapeutic alternatives. Blockade of IL-6 signaling with tocilizumab (TCZ), a humanized monoclonal antibody against IL-6 receptor (IL-6R), represents a newly promising alternative, supported by the results of two recently published clinical trials. However, beyond its implication in the acute phase response, the role of IL-6 in the pathogenesis of GCA and vascular inflammation is still unknown. GCA patients treated with TCZ also showed a decrease of acute-phase proteins, which are usually used to monitor disease activity. Therefore, the utilization of this monoclonal antibody remarks the urgency to find alternative biomarker not directly related with IL-6 signaling to monitor GCA patients treated with TCZ. Considering all this information, the aim of this doctoral thesis was to better understand the role of IL-6 in GCA pathogenesis as well as the impact of IL-6R blockade with TCZ. In addition, we aimed to test the potential of osteopontin (OPN) as a biomarker of disease activity in patients treated with this monoclonal antibody. The results from the present study show that IL-6 and IL-6R are remarkably increased in temporal artery lesions from GCA patients compared with control arteries. Co-culture experiments suggest that vascular smooth muscle cells (VSMC) may be an important source of IL-6. IL-6R was found upregulated in GCA lesions, particularly at the granulomatous areas. Co-culture experiments supported this result since IL-6R protein expression was increased in mononuclear cells when co-cultured with VSMC. Contrary to what was observed in tissue, serum levels of sIL-6R showed no differences between GCA patients and controls. The artery culture model was used to better understand the impact of TCZ. IL-6R blockade resulted in a significant decrease in the mRNA expression of STAT3 and SOCS3 after 5 days in culture. However, phosphorylation levels of STAT3 were not modified by TCZ treatment. Co-culture results suggest that under inflammatory conditions the inhibitory effect of TCZ on STAT3 activation may be partially compensated by alternative mechanisms. IL-6R blockade with TCZ also decreased CCL2 and increased the expression of CXCL9 and CXCL10 in cultured temporal arteries. Based on in vitro results, IL-6R blockade may promote an upregulation of CXCL9 and CXCL10 expression in mononuclear cells, that may explain the increased expression observed in cultured arteries. The upregulation of this chemokines may be due to an increase in STAT1 expression and activation after TCZ treatment. IL-6R blockade with TCZ also induced a reduction in the adhesion and migratory capacity of mononuclear cells. These results suggest that IL-6R blockade with TCZ may contribute to decrease tissue inflammation by limiting the advent of new inflammatory cells. Further research is needed to better understand the molecules involved in TCZ modulation of these processes. TCZ treatment of cultured arteries did not affect OPN expression in GCA lesions. Consistently, while levels of C-reactive protein (CRP) were virtually undetectable after IL- 6R blockade, serum concentration of OPN was similar in patients on glucocorticoid or TCZ maintained remission. All together, these data suggest that sOPN could be a useful biomarker of disease activity for TCZ treated patients. However, the role of sOPN needs to be further explored in larger studies with longitudinal cohorts.
L’arteritis de cèl·lules gegants (ACG) és una malaltia inflamatòria crònica d’etiologia desconeguda que afecta les arteries de mitjà i gran calibre. El tractament actual es basa en l’administració de glucocorticoides tot i que presenten efectes adversos i molts pacients experimenten recaigudes. Aquest fet promou la recerca de teràpies alternatives o complementaries. Recentment, s’han publicat els resultats de dos assajos clínics on s’ha vist que un nou fàrmac anomenat tocilizumab (TCZ), un anticòs que bloqueja el receptor de la IL-6 (IL-6R), podria ser una bona alternativa terapèutica per al pacients amb ACG. No obstant, el paper de la IL-6 en la patogènesi de l’ACG és encara desconegut. A més, l’ús del TCZ ha posat de manifest la necessitat de buscar biomarcadors alternatius als clàssicament utilitzats per monitoritzar els pacients, ja que el tractament amb aquest anticòs redueix l’expressió de les proteïnes de fase aguda, les quals són induïdes per la IL-6. Els objectius de la present tesi doctoral han estat per tant, entendre millor el paper de la IL-6 en l’ACG, així com estudiar l’impacte del bloqueig del IL-6R amb TCZ. Tanmateix, s’ha analitzat el potencial de l’osteopontiona (OPN) com a biomarcador alternatiu en pacients tractats amb aquest anticòs. Els resultats del present estudi mostren que tant la IL-6 com el seu receptor es troben incrementats en les lesions de pacients amb ACG. El bloqueig del IL-6R amb TCZ té un efecte clar sobre l’expressió de les quimiocines CCL2, CXCL9 i CXCL10. A més, els resultats suggereixen que el tractament amb TCZ podria contribuir a disminuir la inflamació en els teixits al prevenir l’arribada de noves cèl·lules inflamatòries. En relació al possible paper de l’OPN com a biomarcador en pacients tractats amb TCZ es va veure que els nivells de OPN en sèrum eren similar als dels pacients tractats amb glucocorticoides. Per contra, els nivells de proteïna C reactiva eren pràcticament indetectables en el grup de pacients tractats amb l’anticòs. En conjunt, els resultats mostren que l’OPN podria ser un bon biomarcador de l’activitat de la malaltia en pacients tractats amb TCZ.

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Fischer, Patrick. "Bedeutung der IL-6-Signaltransduktionsinhibitoren SHP2 und SOCS3 für die Desensitisierung des IL-6-Signalweges". [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=980407699.

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Dawson, Charlotte Helen. "STAT 6 and IL-4 signalling". Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245716.

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Saramago, Eduardo Alves. "O hidrogênio molecular potencializa a hipotermia e previne a hipotensão e a febre durante a inflamação sistêmica induzida por LPS". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17134/tde-07022019-140036/.

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O hidrogênio molecular (H2) exerce efeito antioxidante, anti-apoptótico e antiinflamatório. Nesse estudo testamos a hipótese que o H2 modula as mudanças cardiovasculares, inflamatórias e termorregulatórias na inflamação sistêmica (IS) induzida por lipopolissacarídeo (LPS) em diferentes doses (0,1 ou 1,5 mg/kg, intravenoso, induzindo IS moderada ou severa) em ratos machos Wistar (250-300 g). LPS ou salina foi injetada imediatamente antes do início dos 360 minutos de inalação do H2 (2% H2, 21% O2, balanceado com nitrogênio) ou ar ambiente (21% O2, balanceado com nitrogênio). A temperatura corporal (Tc) foi mensurada por datalogger pré-implantados na cavidade peritoneal. O H2 não causou mudança nos parâmetros cardiovasculares, inflamatórios e na Tc dos ratos controle (tratados com salina). Durante a IS moderada o H2 reduziu o surgimento das citocinas pró-inflamatórias no plasma (TNF-? e IL-6) enquanto causou um aumento da IL-10 plasmática (citocina anti-inflamatória) e preveniu a febre. Durante a IS severa o H2 potencializou a hipotermia e preveniu a febre e a hipotensão. Além disso, o H2 causou uma redução no surgimento das citocinas pró-inflamatórias (TNF-? e IL-1? do plasma) e prostaglandina E2 [(PGE2), no plasma e no hipotálamo], e um aumento da IL-10 plasmática. Esses dados são consistentes com o entendimento que o H2 atenua a febre na IS moderada e durante a IS severa potencializa a hipotermia, previne a hipotensão e exerce um efeito antiinflamatório forte o suficiente para prevenir a febre alterando a sinalização febrigênica e alterando a produção hipotalâmica de PGE2
Molecular hydrogen (H2) exerts anti-oxidative, anti-apoptotic, and anti-inflammatory effects. Here we tested the hypothesis that H2 modulates cardiovascular, inflammatory, and thermoregulatory changes in systemic inflammation (SI) induced by lipopolysaccharide (LPS) at different doses (0.1 or 1.5 mg/kg, intravenously, to induce mild or severe SI) in male Wistar rats (250-300 g). LPS or saline was injected immediately before the beginning of 360- minute inhalation of H2 (2% H2, 21% O2, balanced with nitrogen) or room air (21% O2, balanced with nitrogen). Deep body temperature (Tb) was measured by dataloggers preimplanted in the peritoneal cavity. H2 caused no change in cardiovascular, inflammatory parameters, and Tb of control rats (treated with saline). During mild SI, H2 reduced plasma surges of proinflammatory cytokines (TNF-? and IL-6) while caused an increase in plasma IL-10 (anti-inflammatory cytokine) and prevented fever. During severe SI, H2 potentiated hypothermia, and prevented fever and hypotension. Moreover, H2 caused a reduction in surges of proinflammatory cytokines (plasma TNF-? and IL-1?) and prostaglandin E2 [(PGE2), in plasma and hypothalamus], and an increase in plasma IL-10. These data are consistent with the notion that H2 blunts fever in mild SI, and during severe SI potentiates hypothermia, prevents hypotension and exerts anti-inflammatory effects strong enough to prevent fever by altering febrigenic signaling and ultimately down-modulating hypothalamic PGE2 production

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Denz, Ulrich. "Einfluss des IL-6-sIL-6R-Fusionsproteins Hyper-IL-6 auf die Leber nach hydrodynamischer Transfektion in vivo". [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973066008.

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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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FURINI, Federica. "P2X7 receptor (P2X7R) in Systemic Lupus Erythematosus (SLE). Exploring a novel pathogenetic pathway". Doctoral thesis, Università degli studi di Ferrara, 2019. http://hdl.handle.net/11392/2487988.

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Introduzione. P2X7R è un recettore extracellulare ATP-dipendente coinvolto in processi infiammatori e autoimmuni che agiscono principalmente attraverso l'attivazione dell'inflammasoma NLRP3 e il rilascio di IL-1β, ed anche tramite processi implicati nella regolazione della proliferazione dei linfociti e nell'apoptosi cellulare. Diverse osservazioni da modelli animali e studi su paziente evidenziano un possibile collegamento tra l'asse P2X7R-NLRP3 e la patogenesi del Lupus Eritematoso Sistemico (SLE). L'asse inflammasoma-P2X7R oltre alla produzione diretta di IL-1b e IL-18, è coinvolto indirettamente nel rilascio di altre citochine implicate nella patogenesi di SLE, come IL-6. Lo scopo di questo studio è di esplorare il ruolo di P2X7R e di NLRP3- inflammasoma nel Lupus. Metodi. Sono stati arruolati 48 pazienti con SLE, 16 con (SLE-S) e 32 senza (SLE-NS) anamnesi positiva per sierosite e 20 soggetti di controllo sani (HC) abbinati per sesso ed età. Sono stati raccolti dati demografici, clinici, terapeutici e misure di outcome. I livelli plasmatici di IL-1β e IL-6 sono stati valutati mediante ELISA. Le cellule mononucleate del sangue periferico (PBMC) sono state isolate dal sangue venoso mediante sedimentazione a gradiente di Ficoll e impiegate come segue: 1) valutazione dell'espressione di P2X7R e NLRP3 mediante RT-PCR; 2) determinazione dell'attività P2X7R come incrementi dei livelli di Calcio intracellulare [Ca2 +]i indotti da Benzoyl ATP (BzATP) usando la sonda fluorescente Fura2-AM; 3) isolamento di monociti / macrofagi e valutazione del rilascio in vitro di IL-1β e IL-6 dopo stimolazione con lipopolisaccaride (LPS) e BzATP, separatamente o in combinazione. Risultati. I livelli plasmatici di IL-1β non sono risultati significativamente differenti nei pazienti con SLE rispetto a HC mentre i livelli di IL-6 sono risultati più elevati in SLE rispetto a HC, in modo significativo nei pazienti con storia di sierosite. Monociti / macrofagi isolati da pazienti affetti da SLE rilasciavano quantità inferiori di IL-1β dopo stimolazione con BzATP, mentre il rilascio di IL-6 è risultato significativamente aumentato in SLE-NS rispetto a entrambi i soggetti HC e SLE-S dopo tutti i tipi di stimolazione. L'aumento di [Ca2 +]i dopo stimolazione con BzATP era significativamente più basso nei PBMC di pazienti con SLE rispetto a PBMC da HC. La RT-PCR ha mostrato una riduzione significativa del P2X7R e un'espressione NLRP3 significativamente aumentata nei pazienti rispetto a HC. Conclusioni. I nostri dati indicano una ridotta espressione e funzione di P2X7R nei pazienti affetti da SLE rispetto ai soggetti HC e, al contrario, aumento della segnalazione di IL-6. Le possibili conseguenze della riduzione del P2X7R, principalmente sulla regolazione del network citochinico e sulla proliferazione dei linfociti, dovranno essere ulteriormente approfondite così come il ruolo dell'IL-6 come possibile obiettivo terapeutico, specialmente nei paziente con storia di sierosite.
Introduction. P2X7R is an extracellular ATP-gated receptor involved in inflammatory and autoimmune processes mainly acting through NLPR3-inflammasome activation and IL-1β release, also implicated in lymphocyte proliferation and cellular apoptosis. Several observations from animal models and patient’s studies highlight a possible link between P2X7R-NLRP3 axis and Systemic Lupus Erythematosus (SLE) pathogenesis. The P2X7R-inflammasome axis in addition to the direct production of IL-1 and IL-18, indirectly mediates the release of other cytokines implicated in the pathogenesis of SLE, such as IL-6. The aim of this study was to investigate the role of P2X7R and NLRP3-inflammasome in SLE. Methods. 48 SLE patients, 16 with (SLE-S) and 32 without (SLE-NS) history of serositis, and 20 healthy control (HC) subjects matched for sex and age were enrolled. Demographic, clinical, therapeutic data and outcome measures were collected. IL-1β and IL-6 plasma levels were evaluated by ELISA. Peripheral blood mononuclear cells (PBMCs) were isolated from venous blood by Ficoll gradient sedimentation and employed as follows: 1) evaluation of P2X7R and NLRP3 expression by RT-PCR; 2) determination of P2X7R activity as Benzoyl ATP (BzATP)-induced [Ca2+]i increments using Fura2-AM fluorescent probe; 3) isolation of monocytes/macrophages and assessment of in vitro IL-1β and IL-6 release following stimulation with lipopolysaccharide (LPS) and BzATP, either separately or in combination. Results. Plasma IL-1β levels were unmodified in SLE subjects respect to HC whereas IL-6 levels were higher in SLE than in HC, resulting significantly increased in SLE-S. Monocytes/macrophages isolated from SLE patients released lower quantities of IL-1β after stimulation with BzATP, whereas IL-6 release was significantly augmented in SLE-NS respect to both HC subjects and SLE-S after all types of stimulation. The [Ca2+]i increase following BzATP stimulation was significantly lower in PBMCs from SLE patients than in PBMCs from HC. RT-PCR showed significantly reduced P2X7R and significantly augmented NLRP3 expression in SLE patients. Conclusion. Our data indicate reduced P2X7R expression and function in SLE patients compared with HC subjects and, conversely, increased IL-6 signaling. The possible consequences of reduced P2X7R, mainly on cytokines network deregulation and lymphocyte proliferation, will be further investigated as well as the role of IL-6 as a possible therapeutic target especially in lupus serositis.

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Pereira, Leonardo Costa. "A influência do treinamento excêntrico nos níveis séricos de IL-6 e no polimorfismo -174C/G da IL-6". reponame:Repositório Institucional da UnB, 2013. http://repositorio.unb.br/handle/10482/14374.

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Dissertação (mestrado)—Universidade de Brasília, Programa de Pós Graduação em Ciências da Saúde, 2013.
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Introdução: Com o crescente envelhecimento da população brasileira estratégias que possam contribuir para a manutenção da saúde desse grupo etário são de suma relevância. Assim, estudos que abordam a prática de treino físico e a influencia genética sobre as respostas geradas no organismo de idosos vêm sendo desenvolvidos. Objetivo: A presente pesquisa teve por objetivo avaliar a relação do polimorfismo do gene promotor -174 C/G da IL-6 sobre as respostas da IL-6 sistêmica e dano muscular após treinamento de força excêntrico em homens idosos. Metodologia: Foram determinados os níveis de CK e de IL-6 nos momento pré, 0 h, 3 h, 24 h, 48 horas pós treino excêntrico para homens idosos. Foram identificadas as frequências genicas do polimorfismo do gene promotor IL6 G-174C e foram analisadas as possíveis relações genéticas com os níveis séricos da IL-6 e CK nos diferentes momentos. Para determinação da frequência genotípica foi empregado o teste de Hardy-Weinberg. Para efeito de análise estatística os sujeitos foram divididos em dois grupos genotípicos GG e CC/CG. Os dados contínuos foram expressos em média e erro padrão. Para comparar as medidas de CK e IL-6 foi utilizada ANOVA. As correlações entre o polimorfismo do gene promotor -174 C/G da IL-6 e os resultados de CK, IL-6, lipidograma, idade, altura e composição corporal foram determinadas pelo teste T independente. Resultados: Não foram encontradas diferenças significativas entre os grupos genotípicos e as variáveis antropométricas (p>0,05), perfil lipídico (p>0,05) e CK em todos os momentos (p>0,05). Foram verificadas diferenças entre os níveis de IL-6 basais e pós treino para todos os momentos entre os grupos (p=0,029). Conclusão: O treino excêntrico influenciou na modulação de CK e IL-6 independentemente do Polimorfismo do gene promotor - 174 C/G da IL-6. ______________________________________________________________________________ ABSTRACT
Introduction: With the increasing aging of the Brazilian population, strategies that may contribute to the maintenance of the health of this age group are of supreme importance. Studies what approach the practice of physical training and the genetic influence on the responses generated in the body of the elderly are being developed. Objective: The present research purposed to assess the relationship between polymorphism of the gene promoter -174 C/G from IL-6 about the replies of systemic IL-6 and muscle damage after eccentric strength training in elderly men. Methodology: Were determined the CK and the IL-6 levels in pre moment, 0 h, 3 h, 24 h, 48 hours after eccentric training in elderly men. Were identified the gene frequencies of polymorphism of promoter gene IL6 G-174C and were analyzed the possible genetic relationships with serum levels of IL-6 and CK in different moments. For determination of the genotype frequency was employed the test of Hardy-Weinberg. For the purpose of statistical analysis the subjects were divided into two genotypic groups GG and CC/CG. Continuous data were expressed as average and standard error. To compare the measures of CK and IL-6 it was used ANOVA. The correlations between the polymorphism of the gene promoter -174 C/G of IL-6 and the results of CK, IL-6, lipidogram, age, height and body composition were determined by independent T test. Results: No significant differences were found between the genotypic groups and anthropometric variables (p>0,05), lipid profile (p>0,05) and CK in every moment (p>0,05). Differences were found between the levels of IL-6 basal and after training for all moments about the groups (p=0,029). Conclusion: The eccentric training was influenced in the modulation of CK and IL-6 independently of polymorphism of the gene promoter -174 C/G from IL-6.

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Malchow, Sven [Verfasser]. "Impact of IL-6 classic- and IL-6 trans-signaling on Concanavalin A immune-mediated liver damage / Sven Malchow". Kiel : Universitätsbibliothek Kiel, 2010. http://d-nb.info/102000407X/34.

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Correia, JosÃ Walter. "Polimorfismo -174g>C do gene de Interleucina-6 da Tuberculose Pulmonar". Universidade Federal do CearÃ, 2009. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=3567.

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O objetivo do estudo foi investigar o perfil de produÃÃo de IL-6 em pacientes com tuberculose pulmonar ativa e avaliar o papel funcional do polimorfismo -174G>C do gene de IL-6 na produÃÃo sistÃmica desta citocina. Um total de 63 pacientes e 99 controles foi estudado, sendo 38 pacientes [25(65,8%) masculinos] e 63 controles [51 (81%) masculinos] para a dosagem de IL-6, enquanto, 42 pacientes [25 (60%) masculinos] e 79 controles [62(78,5%) masculinos] para o estudo do polimorfismo. Os pacientes foram selecionados dos centros de referÃncia da rede estadual de saÃde: Dona LibÃnia, Hospital de Messejana, Hospital de MaracanaÃ e Hospital Geral Dr. CÃsar Cals. O grupo controle foi selecionado no HEMOCE. Foi realizado teste de ELISA para a dosagem sÃrica de IL-6. O DNA genÃmico foi extraÃdo de sangue perifÃrico e o polimorfismo de IL-6 foi estudado por reaÃÃo de polimerase em cadeia utilizando iniciadores seqÃÃncia especÃficos. A dosagem sÃrica de IL-6 se mostrou elevada nos pacientes portadores de tuberculose em relaÃÃo aos controles (mediana = 4,3 pg/mL versus 0,5 pg/mL, p<0,001), porÃm nÃo exibiu diferenÃa entre os grupos de doentes sensÃveis e os resistentes ao tratamento especÃfico. Em relaÃÃo ao estudo funcional do polimorismo de IL-6, foi observado um robusto aumento dos nÃveis de IL-6 nos doentes portadores do genÃtipo GG (mediana=4,1 pg/mL, variaÃÃo 0,5-12,0 pg/mL), em relaÃÃo aos portadores dos genÃtipos GC e CC, sendo que nestes se observou uma expressÃo de IL-6 semelhante a dos controles (mediana=0,6 pg/mL, variaÃÃo 0,0-2,8 pg/mL), conferindo significÃncia estatÃstica com p=0,04. A relevÃncia deste estudo Ã mostrar in vivo o papel funcional do polimorfismo de IL-6 na tuberculose. Em conclusÃo, o genÃtipo GG de pacientes com tuberculose pulmonar ativa determina produÃÃo aumentada de IL-6.
The aim of this study was to investigate the profile of IL-6 production in patients with active pulmonary tuberculosis and to evaluate the functional role of polymorphism -174G>C in the systemic production of this cytokine. A total of 63 patients and 99 controls were studied. Among them 38 patients [25(65.8%) males] and 63 controls [51(81%) males] were studied for the IL-6 dosage. Moreover, 42 patients [25(60%) males] and 79 controls [62(78.5%) males] were studied for the -174G>C polymorphism. Patients were selected from Dona LibÃnia Center; Messejana Hospital, Maracanau Hospital and Dr. Cesar Cals General Hospital. The control group was selected from HEMOCE. An ELISA test was performed to measure IL-6 in peripheral blood. The genomic DNA was extracted from peripheral blood and IL-6 polymorphism was studied by polymerase chain reaction using sequence-specific primers. The IL-6 dosage showed an increase in patients with tuberculosis in relation to controls (An increase in IL6 dosage was found in patients with tuberculosis in relation to controls) (median= 4.3 pg/mL vs 0.5 pg/mL, p<0.001), but no difference was observed in drug-sensitive patients in comparison to drug-resistant ones. The genotype distribution showed no difference between patients and controls. In relation to the functional study, the IL-6 levels pointed out a significant increase in patients presenting GG genotype (median=4.1 pg/mL, range 0.5-12.0 pg/mL), in relation to GC and CC careers; these two latter genotypes presented similar IL-6 production as in healthy individuals with median=0.6 pg/mL, range 0.0-2.8 pg/mL, corroborating statistical significance with p=0.04. The relevance of this study is to show in vivo the functional role of IL-6 polymorphism in active pulmonary tuberculosis. Conclusion, the GG genotype in patients with pulmonary tuberculosis determines an increase in IL-6 systemic production.

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Książki na temat "IL-6"

6-il myŏngsang chʻehŏmgi. Sŏul-si: Pulgwang Chʻulpʻanbu, 2000.

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Serena, Bassano, i Montarese Mauro, red. Il teatro di Govi: 6 commedie, 6 successi. Genova: Erga, 1995.

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Yi, Kyŏng-nam. Unmyŏng ŭi kŭ 6-il. Sŏul-si: Palgŭn Maŭm ŭl Kajin Saramdŭl, 1998.

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Yi, Kyŏng-nam. Unmyŏng ŭi kŭ 6-il. Sŏul-si: Palgŭn Maŭm ŭl Kajin Saramdŭl, 1998.

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Yi, Kyŏng-nam. Unmyŏng ŭi kŭ 6-il. Sŏul-si: Palgŭn Maŭm ŭl Kajin Saramdŭl, 1998.

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Francesco, Bonami, Turin (Italy). Galleria civica d'arte moderna e contemporanea., Bonnefantenmuseum i Fondazione Sandretto Re Rebaudengo per l'arte., red. Campo 6: Il villaggio a spirale. Milano: Skira, 1996.

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Gregory, Bock, Marsh Joan i Widdows Kate, red. Polyfunctional cytokines: IL-6 and LIF. Chichester, Eng: Wiley, 1992.

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Michel, Revel, red. IL-6: Physiopathology and clinical potentials. New York: Raven Press, 1992.

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Hyŏphoe, Hanʼguk Ko Misul, red. Chosŏn munbang popʻumjŏn, 6-wŏl 1-il--7-il Paegak Misulgwan. [Seoul]: Hanʼguk Ko Misul Hyŏphoe, 1989.

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Baj, Enrico, i Mario Logli. Mario Logli: Raccontare il futuro : 6 percorsi immaginati. Roma: Comitato europeo "Giacomo Leopardi,", 1987.

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Części książek na temat "IL-6"

Rohleder, Nicolas. "Interleukins, -1 (IL-1), -6 (IL-6), -18 (IL-18)". W Encyclopedia of Behavioral Medicine, 1210–12. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_26.

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Boltz, Marie, Holly Rau, Paula Williams, Holly Rau, Paula Williams, Jane Upton, Jos A. Bosch i in. "Interleukins, -1 (IL-1), -6 (IL-6), -18 (IL-18)". W Encyclopedia of Behavioral Medicine, 1092–94. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_26.

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Tanaka, Toshio, Masashi Narazaki i Tadamistu Kishimoto. "IL-6 Superfamily". W Inflammation - From Molecular and Cellular Mechanisms to the Clinic, 573–86. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527692156.ch23.

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Suematsu, S., M. Hibi, T. Sugita, M. Saito, M. Murakami, T. Matsusaka, T. Matsuda, T. Hirano, T. Taga i T. Kishimoto. "Interleukin 6 (IL-6) and Its Receptor (IL-6R) in Myeloma/Plasmacytoma". W Current Topics in Microbiology and Immunology, 13–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75889-8_2.

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Mir, Manzoor Ahmad, Masrat Bashir i Nusrat Jan. "The Role of Interleukin (IL)-6/IL-6 Receptor Axis in Cancer". W Cytokine and Chemokine Networks in Cancer, 137–64. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-4657-0_5.

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Kamimura, Daisuke, Yasunobu Arima, Toshio Hirano, Hideki Ogura i Masaaki Murakami. "IL-6 and Inflammatory Diseases". W Cytokine Frontiers, 53–78. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54442-5_2.

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Fairuz i Humaryanto. "Immunoexpression of Interleukin-6 (Il-6) in Keloid". W Proceedings of the 4th Green Development International Conference (GDIC 2022), 1081–87. Paris: Atlantis Press SARL, 2023. http://dx.doi.org/10.2991/978-2-38476-110-4_104.

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Grötzinger, J. "IL-6 Type Cytokine Receptor Complexes". W Insulin & Related Proteins - Structure to Function and Pharmacology, 201–12. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/0-306-47582-0_16.

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Nishimoto, Norihiro, i Tadamitsu Kishimoto. "Is IL-6 a therapeutic target?" W Cytokines and Joint Injury, 89–106. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7883-8_4.

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Vuotto, M. L., A. Barbarisi, E. Bresciano, M. Fratta, M. T. Ielpo, M. Mosti i D. Mancino. "IL-6 Changes After Surgical Stress". W Immunology and Its Impact on Infections in Surgery, 159–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79079-9_21.

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Streszczenia konferencji na temat "IL-6"

Pauwels, NS, KR Bracke, GF Joos i GG Brusselle. "IL-6 Family of Cytokines in Lungs of Cigarette Smoke Exposed Wildtype and IL-6 Knockout Mice." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1322.

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Johnston, James B., Ju-Yoon Yoon, Sunjay Lakhi, Brenda Kuschak, Donna Hewitt i Spencer B. Gibson. "Abstract 1762: Clinical relevance of plasma IL-6 and IL-6 levels in chronic lymphocytic leukemia (CLL)". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1762.

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Paulino do Prado, Thaís, ELIANA PEREIRA DE ARAUJO, VANESSA CRISTINA DIAS BÓBBO, ALBINA DE FÁTIMA SILVA RAMALHO i JOSEANE MORARI. "CARACTERIZAÇÃO DA EXPRESSÃO DA INTERLEUCINA-6 (IL-6) EM NEURÔNIOS HIPOTALÂMICOS". W XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil: Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-51404.

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Mohammed, Alia Hashim, i Areej Atiyah Hussein. "Possible role of IL-6 and IL-17 among COVID-19 patients". W 2ND INTERNATIONAL CONFERENCE ON MATHEMATICAL TECHNIQUES AND APPLICATIONS: ICMTA2021. AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0103903.

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Conway, M., D. Francisco, A. Hurbon, J. Gozdz, H. W. Chu, J. G. Ledford i M. Kraft. "Surfactant Protein A Modulates IL-13 and IL-6 Phosphorylation of STAT3". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2911.

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Voigt, Christoph, Marion Kubitza, Rania Dayoub, Michael Melter i Thomas S. Weiss. "IL-6 receptor availability and IL-6/STAT3 signal transduction is regulated by ALR through altered sheddase ADAM17". W 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777478.

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Dimitrova, Denitsa, Vania Youroukova, Tsvetelina Velikova i Kalina Tumangelova-Yuzeir. "Serum levels of IL-5, IL-6 and IL-8 in moderate and severe asthma clusters". W ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa5060.

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Eikawa, Shingo, Yoshihiro Ohue, Kenta Kitaoka, Toshiki Aji, Akiko Uenaka, Mikio Oka i Eiichi Nakayama. "Abstract 1915: Enrichment of Tregs in migrated T-cells to IL-6- and IL-8-expressing tumors through induction of CXCR1 by IL-6". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1915.

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Johansson, M. W., M. C. Tattersall, S. J. Esnault, K. E. Lee, H. L. Floerke, J. Heebink, E. A. Townsend i in. "High Airway Interleukin (IL)-6 Is Associated With Increased Blood IL-6 in Asthma Following Segmental Bronchoprovocation With Allergen". W American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a6983.

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Gollnick, Sandra O., David A. Musser i Barbara W. Henderson. "Photodynamic therapy affects the expression of IL-6 and IL-10 in vivo". W BiOS '98 International Biomedical Optics Symposium, redaktor Steven L. Jacques. SPIE, 1998. http://dx.doi.org/10.1117/12.308168.

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Raporty organizacyjne na temat "IL-6"

Li, Chenglong, James Fuchs i Jiayuh Lin. Novel Small Molecules Disabling the IL-6/IL-6R/GP130 Heterohexamer Complex. Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada606135.

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Waltz, Susan E. IL-6 Receptor Isoforms and Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2013. http://dx.doi.org/10.21236/ada575873.

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Waltz, Susan E. IL-6 Receptor Isoforms and Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, październik 2011. http://dx.doi.org/10.21236/ada601956.

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Drew, Angela F. IL-6 Receptor Isoforms and Ovarian Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, październik 2010. http://dx.doi.org/10.21236/ada552118.

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Levine, Alice. Effect of COX-2 (PGE2) and IL-6 on Prostate Bone Metastases. Fort Belvoir, VA: Defense Technical Information Center, luty 2006. http://dx.doi.org/10.21236/ada448615.

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Levine, Alice C. Effect of COX-2 (PGE2) and IL-6 on Prostate Cancer Bone Mets. Fort Belvoir, VA: Defense Technical Information Center, luty 2007. http://dx.doi.org/10.21236/ada466562.

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Levine, Alice C. Effect of COX-2 (PGE2) and IL-6 on Prostate Cancer Bone Metastases. Fort Belvoir, VA: Defense Technical Information Center, luty 2008. http://dx.doi.org/10.21236/ada481330.

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Jafrin, Sarah, Md Abdul Aziz i Mohammad Safiqul Islam. Elevated levels of pleiotropic interleukin-6 (IL-6) and interleukin-10 (IL-10) are critically involved with the severity and mortality of COVID-19: An updated longitudinal meta-analysis and systematic review on 147 studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2022. http://dx.doi.org/10.37766/inplasy2022.4.0046.

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Review question / Objective: How were serum IL-6 and IL-10 linked with the severity and mortality of COVID-19 patients? To evaluate the role of IL-6 and IL-10 in the development of the severity or morality of COVID-19 patients. The outcomes (mean difference) were calculated between the severe vs. non-severe COVID-19 patients and non-survival vs. survival patients to evaluate the risk of severity or mortality. Condition being studied: Severity and mortality among the COVID-19 patients. Information sources: The international scientific authorized databases such as Google Scholar, PubMed, Embase, CNKI, Cochrane Library, and Web of science were used as primary sources to identify and collect the eligible literature. Additional secondary databases were also comprehensively searched to extract more related studies.

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Wang, Zhenhu. Efficacy and safety of different IL-6 inhibitors in COVID-19: a network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2021. http://dx.doi.org/10.37766/inplasy2021.4.0007.

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