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[PMID]:29441967
[Au] Autor:Sheng F; Han M; Huang Z; Zhang L
[Ti] Título:Interleukin 6 receptor inhibitor tocilizumab suppresses cytokine expression, inflammasome activation and phagocytosis in a cell model of sepsis.
[So] Source:Pharmazie;71(11):636-639, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Sepsis is a life-threatening condition, usually accompanied by excessive inflammation. Tocilizumab (TCZ) is a humanized monoclonal antibody against the interleukin (IL) 6 receptor and has been studied in various inflammatory diseases, but little is known about its effects in sepsis. This study aims to reveal the role of TCZ in inflammation during sepsis. METHODS: Human monocyte cell line THP-1 was stimulated by lipopolysaccharide (LPS) as a cell model for sepsis. After TCZ treatment, the expression of cytokines tumor necrosis factor (TNF) and IL10, the production of chemokine (C-C motif) ligand 2 (CCL2) and IL1B, and the expression of inflammasome factors NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1), were detected by qRT-PCR and ELISA. Phagocytosis assay was also performed to assess the phagocytosis activity of TCZ-treated cells. RESULTS: LPS stimulation significantly upregulated TNF and IL10 mRNA levels (P < 0.01) and CCL2 and IL1B production (P < 0.001), promoted NLRP3 and CASP1 levels (P < 0.01) and elevated phagocytosis activity of THP-1 cells (P < 0.001). TCZ treatment had the opposite effects of decreasing TNF and IL10 mRNA levels (P < 0.05), CCL2 and IL1B production (P < 0.001), inhibiting NLRP3 and CASP1 (P < 0.01), and suppressing phagocytosis activity (P < 0.001) compared to the LPS group. CONCLUSION: These results indicate the suppressive role of TCZ in cytokine production, inflammation activation and phagocytosis in sepsis cell model, implying its effects on controlling "cytokine storm" during sepsis. Thus TCZ provides a promising strategy for treating sepsis.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/farmacologia
Citocinas/antagonistas & inibidores
Inflamassomos/efeitos dos fármacos
Fagocitose/efeitos dos fármacos
Receptores de Interleucina-6/antagonistas & inibidores
Sepse/patologia
[Mh] Termos MeSH secundário: Linhagem Celular
Citocinas/biossíntese
Seres Humanos
Lipopolissacarídeos/antagonistas & inibidores
Lipopolissacarídeos/farmacologia
Monócitos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Cytokines); 0 (Inflammasomes); 0 (Lipopolysaccharides); 0 (Receptors, Interleukin-6); I031V2H011 (tocilizumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6713


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[PMID]:28745999
[Au] Autor:Stone JH; Tuckwell K; Dimonaco S; Klearman M; Aringer M; Blockmans D; Brouwer E; Cid MC; Dasgupta B; Rech J; Salvarani C; Schett G; Schulze-Koops H; Spiera R; Unizony SH; Collinson N
[Ad] Endereço:From the Massachusetts General Hospital Rheumatology Unit, Harvard Medical School, Boston (J.H.S., S.H.U.); Roche Products, Welwyn Garden City (K.T., S.D., N.C.), and Southend University Hospital NHS Foundation Trust, Westcliff-on-Sea (B.D.) - both in the United Kingdom; Genentech, South San Francis
[Ti] Título:Trial of Tocilizumab in Giant-Cell Arteritis.
[So] Source:N Engl J Med;377(4):317-328, 2017 07 27.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Giant-cell arteritis commonly relapses when glucocorticoids are tapered, and the prolonged use of glucocorticoids is associated with side effects. The effect of the interleukin-6 receptor alpha inhibitor tocilizumab on the rates of relapse during glucocorticoid tapering was studied in patients with giant-cell arteritis. METHODS: In this 1-year trial, we randomly assigned 251 patients, in a 2:1:1:1 ratio, to receive subcutaneous tocilizumab (at a dose of 162 mg) weekly or every other week, combined with a 26-week prednisone taper, or placebo combined with a prednisone taper over a period of either 26 weeks or 52 weeks. The primary outcome was the rate of sustained glucocorticoid-free remission at week 52 in each tocilizumab group as compared with the rate in the placebo group that underwent the 26-week prednisone taper. The key secondary outcome was the rate of remission in each tocilizumab group as compared with the placebo group that underwent the 52-week prednisone taper. Dosing of prednisone and safety were also assessed. RESULTS: Sustained remission at week 52 occurred in 56% of the patients treated with tocilizumab weekly and in 53% of those treated with tocilizumab every other week, as compared with 14% of those in the placebo group that underwent the 26-week prednisone taper and 18% of those in the placebo group that underwent the 52-week prednisone taper (P<0.001 for the comparisons of either active treatment with placebo). The cumulative median prednisone dose over the 52-week period was 1862 mg in each tocilizumab group, as compared with 3296 mg in the placebo group that underwent the 26-week taper (P<0.001 for both comparisons) and 3818 mg in the placebo group that underwent the 52-week taper (P<0.001 for both comparisons). Serious adverse events occurred in 15% of the patients in the group that received tocilizumab weekly, 14% of those in the group that received tocilizumab every other week, 22% of those in the placebo group that underwent the 26-week taper, and 25% of those in the placebo group that underwent the 52-week taper. Anterior ischemic optic neuropathy developed in one patient in the group that received tocilizumab every other week. CONCLUSIONS: Tocilizumab, received weekly or every other week, combined with a 26-week prednisone taper was superior to either 26-week or 52-week prednisone tapering plus placebo with regard to sustained glucocorticoid-free remission in patients with giant-cell arteritis. Longer follow-up is necessary to determine the durability of remission and safety of tocilizumab. (Funded by F. Hoffmann-La Roche; ClinicalTrials.gov number, NCT01791153 .).
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Arterite de Células Gigantes/tratamento farmacológico
Glucocorticoides/administração & dosagem
Prednisona/administração & dosagem
Receptores de Interleucina-6/antagonistas & inibidores
[Mh] Termos MeSH secundário: Idoso
Anticorpos Monoclonais Humanizados/efeitos adversos
Método Duplo-Cego
Esquema de Medicação
Quimioterapia Combinada
Feminino
Glucocorticoides/efeitos adversos
Seres Humanos
Injeções Subcutâneas
Masculino
Meia-Idade
Prednisona/efeitos adversos
Indução de Remissão
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Glucocorticoids); 0 (Receptors, Interleukin-6); 0 (interleukin-6 receptor alpha); I031V2H011 (tocilizumab); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170727
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1613849


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[PMID]:28982132
[Au] Autor:Nishihara M; Aoki H; Ohno S; Furusho A; Hirakata S; Nishida N; Ito S; Hayashi M; Imaizumi T; Fukumoto Y
[Ad] Endereço:Division of Cardiovascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.
[Ti] Título:The role of IL-6 in pathogenesis of abdominal aortic aneurysm in mice.
[So] Source:PLoS One;12(10):e0185923, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although the pathogenesis of abdominal aortic aneurysm (AAA) remains unclear, evidence is accumulating to support a central role for inflammation. Inflammatory responses are coordinated by various soluble cytokines of which IL-6 is one of the major proinflammatory cytokines. In this study we examined the role of IL-6 in the pathogenesis of experimental AAA induced by a periaortic exposure to CaCl2 in mice. We now report that the administration of MR16-1, a neutralizing monoclonal antibody specific for the mouse IL-6 receptor, mildly suppressed the development of AAA. The inhibition of IL-6 signaling provoked by MR16-1 also resulted in a suppression of Stat3 activity. Conversely, no significant changes in either NFκB activity, Jnk activity or the expression of matrix metalloproteinases (Mmp) -2 and -9 were identified. Transcriptome analyses revealed that MR16-1-sensitive genes encode chemokines and their receptors, as well as factors that regulate vascular permeability and cell migration. Imaging cytometric analyses then consistently demonstrated reduced cellular infiltration for MR16-1-treated AAA. These results suggest that IL-6 plays an important but limited role in AAA pathogenesis, and primarily regulates cell migration and infiltration. These data would also suggest that IL-6 activity may play an important role in scenarios of continuous cellular infiltration, possibly including human AAA.
[Mh] Termos MeSH primário: Aneurisma da Aorta Abdominal/fisiopatologia
Interleucina-6/fisiologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/imunologia
Modelos Animais de Doenças
Camundongos
Receptores de Interleucina-6/imunologia
Transdução de Sinais
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Interleukin-6); 0 (Receptors, Interleukin-6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185923


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[PMID]:28981818
[Au] Autor:Shiels MS; Shu XO; Chaturvedi AK; Gao YT; Xiang YB; Cai Q; Hu W; Shelton G; Ji BT; Pinto LA; Kemp TJ; Rothman N; Zheng W; Hildesheim A; Lan Q
[Ad] Endereço:Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD, USA.
[Ti] Título:A prospective study of immune and inflammation markers and risk of lung cancer among female never smokers in Shanghai.
[So] Source:Carcinogenesis;38(10):1004-1010, 2017 Oct 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:There is a paucity of data on risk factors for lung cancer among never smokers. Here, we have carried out the first large study of circulating inflammation markers and lung cancer risk among female never smokers in Shanghai. A study of 248 lung cancer cases in female never smokers and 263 controls was nested within the Shanghai Women's Health Study (n = 75221), matched by dates of birth and blood collection (mean follow-up time = 7.5 years). Prediagnostic plasma levels of 65 inflammation markers were measured using a Luminex bead-based assay. Odds ratios (ORs) were estimated with multivariable logistic regression. Nine of 61 evaluable markers were statistically significantly associated with lung cancer risk among never smoking Chinese women (P-trend across categories <0.05). Soluble interleukin-6 receptor [sIL-6R; highest versus lowest category OR = 2.37; 95% confidence interval (CI) 1.40-4.02) and chemokine (C-C motif) ligand 2/monocyte chemotactic protein 1; (OR = 1.62; 95% CI 0.94-2.80) were associated with an increased risk of lung cancer, whereas interleukin (IL)-21 (OR = 0.53; 95%CI 0.31-0.93), chemokine (C-X3-C motif) ligand 1/fractalkine (OR = 0.54; 95% CI 0.30-0.96), soluble vascular endothelial growth factor receptor 2 (sVEGFR2, OR = 0.45; 95% CI 0.26-0.76), sVEGFR3 (OR = 0.53; 95% CI 0.32-0.90), soluble tumor necrosis factor receptor I (OR = 0.49; 95% CI 0.29-0.83), IL-10 (OR = 0.60; 95% CI 0.34-1.05) and C-reactive protein (OR = 0.63; 95% CI 0.37-1.06) were associated with a decreased risk. sIL-6R remained significantly associated with lung cancer risk >7.5 years prior to diagnosis. Markers involved in various aspects of the immune response were associated with subsequent lung cancer risk, implicating inflammation in the etiology of lung cancer among female never smokers.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Inflamação/metabolismo
Neoplasias Pulmonares/etiologia
Fumar/efeitos adversos
[Mh] Termos MeSH secundário: Proteínas da Fase Aguda/análise
Adulto
Idoso
Biomarcadores/metabolismo
Biomarcadores Tumorais/sangue
Biomarcadores Tumorais/metabolismo
Estudos de Casos e Controles
Quimiocina CX3CL1/sangue
Quimiocinas/sangue
China
Citocinas/sangue
Feminino
Seres Humanos
Inflamação/imunologia
Neoplasias Pulmonares/imunologia
Meia-Idade
Estudos Prospectivos
Receptores de Interleucina-6/sangue
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acute-Phase Proteins); 0 (Biomarkers); 0 (Biomarkers, Tumor); 0 (CX3CL1 protein, human); 0 (Chemokine CX3CL1); 0 (Chemokines); 0 (Cytokines); 0 (Receptors, Interleukin-6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx075


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[PMID]:28953986
[Au] Autor:Chen Y; Yang S; Peng Y; Yang Z
[Ad] Endereço:Department of Infectious Diseases, Linyi People's Hospital, Linyi, Shandong, China.
[Ti] Título:The regulatory role of IL-6R in hepatitis B-associated fibrosis and cirrhosis.
[So] Source:Braz J Med Biol Res;50(11):e6246, 2017 Sep 21.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:This study investigated the expression and regulation of IL-6R in hepatitis B-associated moderate hepatic fibrosis and cirrhosis. Liver tissues, peripheral blood monocytes (PBMs) and serum were collected from 26 hepatitis B patients with liver fibrosis and 35 hepatitis B patients with liver cirrhosis. The levels of Il-6r mRNA expression in these samples were examined by quantitative real-time PCR and IL-6R protein levels were analyzed by western blot and ELISA. MiRNAs that regulate IL-6R expression were predicted by bioinformatics analysis, and validated by dual luciferase reporter assay. Compared with the hepatic fibrosis group, IL-6R was significantly upregulated at both mRNA and protein levels in liver tissues, PBMs and serum samples from the hepatic cirrhosis group (P<0.05). The 3'UTR of Il-6r mRNA was predicted to contain a miR-30b binding site and IL-6R was identified as a possible target of miR-30b. MiR-30b expression was significantly downregulated in samples from hepatic cirrhosis patients compared with hepatic fibrosis patients (P<0.05). In conclusion, IL-6R was upregulated while miR-30b was decreased in patients with liver cirrhosis. The miR-30 can directly regulate the expression of IL-6R.
[Mh] Termos MeSH primário: Hepatite B/metabolismo
Cirrose Hepática/metabolismo
MicroRNAs/metabolismo
Receptores de Interleucina-6/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Adulto
Idoso
Regulação para Baixo
Feminino
Hepatite B/sangue
Seres Humanos
Cirrose Hepática/sangue
Masculino
MicroRNAs/análise
MicroRNAs/química
Meia-Idade
Receptores de Interleucina-6/análise
Valores de Referência
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MIRN30 microRNA, human); 0 (MicroRNAs); 0 (Receptors, Interleukin-6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE


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[PMID]:28877252
[Au] Autor:Link MA; Lücke K; Schmid J; Schumacher V; Eden T; Rose-John S; Mittrücker HW
[Ad] Endereço:Institute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:The role of ADAM17 in the T-cell response against bacterial pathogens.
[So] Source:PLoS One;12(9):e0184320, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ADAM17 is a member of the A Disintegrin And Metalloproteinase family of proteases. It is ubiquitously expressed and causes the shedding of a broad spectrum of surface proteins such as adhesion molecules, cytokines and cytokine receptors. By controlled shedding of these proteins from leukocytes, ADAM17 is able to regulate immune responses. Several ADAM17 targets on T cells have been implicated in T-cell migration, differentiation and effector functions. However, the role of ADAM17 in T-cell responses is still unclear. To characterize the function of ADAM17 in T cells, we used Adam17fl/fl×CD4cre+ mice with a T-cell restricted inactivation of the Adam17 gene. Upon stimulation, ADAM17-deficient CD4+ and CD8+ T cells were impaired in shedding of CD62L, IL-6Rα, TNF-α, TNFRI and TNFRII. Surprisingly, we could not detect profound changes in the composition of major T-cell subsets in Adam17fl/fl×CD4cre+ mice. Following infection with Listeria monocytogenes, Adam17fl/fl×CD4cre+ mice mounted regular listeria-specific CD4+ TH1 and CD8+ T-cell responses and were able to control primary and secondary infections. In conclusion, our study indicates that ADAM17 is either not required in T cells under homoeostatic conditions and for control of listeria infection or can be effectively compensated by other mechanisms.
[Mh] Termos MeSH primário: Proteína ADAM17/metabolismo
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Listeriose/imunologia
[Mh] Termos MeSH secundário: Animais
Adesão Celular
Diferenciação Celular
Membrana Celular/metabolismo
Feminino
Selectina L/metabolismo
Listeria monocytogenes
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptores de Interleucina-6/metabolismo
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Receptores Tipo II do Fator de Necrose Tumoral/metabolismo
Células Th1/imunologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interleukin-6); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Tumor Necrosis Factor-alpha); 126880-86-2 (L-Selectin); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (Adam17 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184320


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[PMID]:28859336
[Au] Autor:Donson AM; Apps J; Griesinger AM; Amani V; Witt DA; Anderson RCE; Niazi TN; Grant G; Souweidane M; Johnston JM; Jackson EM; Kleinschmidt-DeMasters BK; Handler MH; Tan AC; Gore L; Virasami A; Gonzalez-Meljem JM; Jacques TS; Martinez-Barbera JP; Foreman NK; Hankinson TC; Advancing Treatment for Pediatric Craniopharyngioma Consortium
[Ad] Endereço:Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado; Developmental Biology and Cancer Programme, Great Ormond Street UCL Institute of Child Health, London, UK; Department of Neurological Surgery, Columbia University Medical Center, New York, New York; Division
[Ti] Título:Molecular Analyses Reveal Inflammatory Mediators in the Solid Component and Cyst Fluid of Human Adamantinomatous Craniopharyngioma.
[So] Source:J Neuropathol Exp Neurol;76(9):779-788, 2017 Sep 01.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pediatric adamantinomatous craniopharyngioma (ACP) is a highly solid and cystic tumor, often causing substantial damage to critical neuroendocrine structures such as the hypothalamus, pituitary gland, and optic apparatus. Paracrine signaling mechanisms driving tumor behavior have been hypothesized, with IL-6R overexpression identified as a potential therapeutic target. To identify potential novel therapies, we characterized inflammatory and immunomodulatory factors in ACP cyst fluid and solid tumor components. Cytometric bead analysis revealed a highly pro-inflammatory cytokine pattern in fluid from ACP compared to fluids from another cystic pediatric brain tumor, pilocytic astrocytoma. Cytokines and chemokines with particularly elevated concentrations in ACPs were IL-6, CXCL1 (GRO), CXCL8 (IL-8) and the immunosuppressive cytokine IL-10. These data were concordant with solid tumor compartment transcriptomic data from a larger cohort of ACPs, other pediatric brain tumors and normal brain. The majority of receptors for these cytokines and chemokines were also over-expressed in ACPs. In addition to IL-10, the established immunosuppressive factor IDO-1 was overexpressed by ACPs at the mRNA and protein levels. These data indicate that ACP cyst fluids and solid tumor components are characterized by an inflammatory cytokine and chemokine expression pattern. Further study regarding selective cytokine blockade may inform novel therapeutic interventions.
[Mh] Termos MeSH primário: Craniofaringioma/metabolismo
Líquido Cístico/metabolismo
Citocinas/metabolismo
Neoplasias Hipofisárias/metabolismo
[Mh] Termos MeSH secundário: Criança
Pré-Escolar
Estudos de Coortes
Craniofaringioma/genética
Craniofaringioma/patologia
Líquido Cístico/imunologia
Feminino
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica/fisiologia
Seres Humanos
Indolamina-Pirrol 2,3,-Dioxigenase/genética
Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo
Masculino
Análise em Microsséries
Neoplasias Hipofisárias/genética
Neoplasias Hipofisárias/patologia
RNA Mensageiro/metabolismo
Receptores de Interleucina-6/genética
Receptores de Interleucina-6/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Cytokines); 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 0 (RNA, Messenger); 0 (Receptors, Interleukin-6); 0 (indoleamine 2,3-dioxygenase 1, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1093/jnen/nlx061


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[PMID]:28821622
[Au] Autor:Foreman HC; Armstrong J; Santana AL; Krug LT; Reich NC
[Ad] Endereço:From the Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York 11794.
[Ti] Título:The replication and transcription activator of murine gammaherpesvirus 68 cooperatively enhances cytokine-activated, STAT3-mediated gene expression.
[So] Source:J Biol Chem;292(39):16257-16266, 2017 Sep 29.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gammaherpesviruses (γHVs) have a dynamic strategy for lifelong persistence, involving productive infection, latency, and intermittent reactivation. In latency reservoirs, such as B lymphocytes, γHVs exist as viral episomes and express few viral genes. Although the ability of γHV to reactivate from latency and re-enter the lytic phase is challenging to investigate and control, it is known that the γHV replication and transcription activator (RTA) can promote lytic reactivation. In this study, we provide first evidence that RTA of murine γΗV68 (MHV68) selectively binds and enhances the activity of tyrosine-phosphorylated host STAT3. STAT3 is a transcription factor classically activated by specific tyrosine 705 phosphorylation (pTyr -STAT3) in response to cytokine stimulation. pTyr -STAT3 forms a dimer that avidly binds a consensus target site in the promoters of regulated genes, and our results indicate that RTA cooperatively enhances the ability of pTyr -STAT3 to induce expression of a STAT3-responsive reporter gene. As indicated by coimmunoprecipitation, in latently infected B cells that are stimulated to reactivate MHV68, RTA bound specifically to endogenous pTyr -STAT3. An binding assay confirmed that RTA selectively recognizes pTyr -STAT3 and indicated that the C-terminal transactivation domain of RTA was required for enhancing STAT3-directed gene expression. The cooperation of these transcription factors may influence both viral and host genes. During MHV68 infection, pTyr -STAT3 promoted the temporal expression of ORF59, a viral replication protein. Our results demonstrate that MHV68 RTA specifically recognizes and recruits activated pTyr -STAT3 during the lytic phase of infection.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Regulação da Expressão Gênica
Proteínas Imediatamente Precoces/metabolismo
Interleucina-6/metabolismo
Receptores de Interleucina-6/agonistas
Rhadinovirus/fisiologia
Fator de Transcrição STAT3/agonistas
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Linfócitos B/imunologia
Linfócitos B/virologia
Linhagem Celular
Dimerização
Genes Reporter
Seres Humanos
Proteínas Imediatamente Precoces/química
Proteínas Imediatamente Precoces/genética
Camundongos
Mutação
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Fosforilação
Domínios e Motivos de Interação entre Proteínas
Processamento de Proteína Pós-Traducional
Receptores de Interleucina-6/metabolismo
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Rhadinovirus/imunologia
Fator de Transcrição STAT3/química
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Transativadores/química
Transativadores/genética
Tirosina/metabolismo
Ativação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immediate-Early Proteins); 0 (Interleukin-6); 0 (Peptide Fragments); 0 (Receptors, Interleukin-6); 0 (Recombinant Fusion Proteins); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (Trans-Activators); 0 (gene 50 protein, gammaherpesvirus 68); 42HK56048U (Tyrosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.786970


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[PMID]:28753646
[Au] Autor:Van Dyke AL; Lang Kuhs KA; Shiels MS; Koshiol J; Trabert B; Loftfield E; Purdue MP; Wentzensen N; Pfeiffer RM; Katki HA; Hildesheim A; Kemp TJ; Pinto LA; Chaturvedi AK; Safaeian M
[Ad] Endereço:Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, United States of America.
[Ti] Título:Associations between self-reported diabetes and 78 circulating markers of inflammation, immunity, and metabolism among adults in the United States.
[So] Source:PLoS One;12(7):e0182359, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation is increasingly thought to be associated with diabetes; however, only a few inflammation markers have been assessed concurrently in relation to history of diabetes. In the most comprehensive evaluation of inflammation markers and diabetes to date using a Luminex bead-based assay, we measured 78 inflammation-, immune-, and metabolic-related markers detectable in at least 10% of serum samples collected from participants from the Prostate, Lung, Colorectal and Ovarian Cancer (PLCO) screening trial (n = 1,814). At baseline, 6.6% (n = 120) of PLCO participants self-reported a history of diabetes. Cross-sectional associations between these markers and self-reported diabetes were assessed using weighted logistic regression adjusting for sex, smoking status, blood draw age and year, body mass index, and cohort sub-study. Including chemokines [C-C motif ligand (CCL) 19, CCL20, CCL21, C-X-C motif ligand (CXCL) 6, CXCL10, and CXCL11] and soluble cytokine and chemokine receptors [soluble (s) interleukin (IL) 6 receptor (R), soluble tumor necrosis factor receptor (sTNFR) 1, sTNFR2, and sIL-R2], ten inflammation-related markers, were nominally associated with diabetes (P<0.05). In addition to these associations, higher levels of insulin, gastric inhibitory polypeptide, and pancreatic polypeptide remained significantly associated with self-reported diabetes with a false discovery rate <5%, indicating that the assay was able to detect markers associated with diabetes. In summary, self-reported diabetes was nominally associated with circulating cytokines, chemokines, and soluble cytokine and chemokine receptors in the most expansive examination of diabetes and inflammation- and immune-related markers to date. These results highlight the need to explore in future prospective studies the role of inflammation markers in diabetes.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Diabetes Mellitus/sangue
[Mh] Termos MeSH secundário: Idoso
Proteína C-Reativa/metabolismo
Quimiocinas/sangue
Quimiocinas/imunologia
Estudos Transversais
Diabetes Mellitus/imunologia
Diabetes Mellitus/metabolismo
Metabolismo Energético/imunologia
Feminino
Seres Humanos
Inflamação/sangue
Inflamação/imunologia
Interleucina-6/metabolismo
Modelos Logísticos
Masculino
Meia-Idade
Receptores de Interleucina-6/metabolismo
Autorrelato
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Chemokines); 0 (Interleukin-6); 0 (Receptors, Interleukin-6); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182359


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[PMID]:28675418
[Au] Autor:Rose-John S
[Ad] Endereço:Institute of Biochemistry, University of Kiel, Germany.
[Ti] Título:The Soluble Interleukin 6 Receptor: Advanced Therapeutic Options in Inflammation.
[So] Source:Clin Pharmacol Ther;102(4):591-598, 2017 Oct.
[Is] ISSN:1532-6535
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin (IL)-6 binds to IL-6R and the complex of IL-6 and IL-6R associates with the receptor subunit gp130, which initiates signaling. gp130 is expressed on all cells. IL-6R is cleaved by the ADAM17, generating a soluble IL-6R (sIL-6R). The sIL-6R binds IL-6 and the complex of IL-6 and sIL-6R binds to gp130 even on cells that do not express IL-6R. This process, which has been called IL-6 trans-signaling, increases the spectrum of target cells for IL-6. We generated a protein, sgp130Fc, which inhibits IL-6 trans-signaling without affecting IL-6 classic signaling. Using the sgp130Fc protein we demonstrated that IL-6 classic signaling is antiinflammatory and protective, whereas IL-6 trans-signaling is proinflammatory. Blocking IL-6 trans-signaling does not compromise the defense of the body against bacterial infections. We suggest that sgp130Fc is a superior agent as compared to IL-6 or IL-6R antibodies to block IL-6. The sgp130Fc protein is in phase II clinical trials.
[Mh] Termos MeSH primário: Inflamação/tratamento farmacológico
Interleucina-6/metabolismo
Receptores de Interleucina-6/metabolismo
Proteínas Recombinantes de Fusão/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Receptor gp130 de Citocina/metabolismo
Desenho de Drogas
Seres Humanos
Inflamação/imunologia
Inflamação/patologia
Interleucina-6/imunologia
Receptores de Interleucina-6/imunologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Interleukin-6); 0 (Receptors, Interleukin-6); 0 (Recombinant Fusion Proteins); 0 (Sgp130Fc protein); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1002/cpt.782



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