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[PMID]:29191879
[Au] Autor:Engblom C; Pfirschke C; Zilionis R; Da Silva Martins J; Bos SA; Courties G; Rickelt S; Severe N; Baryawno N; Faget J; Savova V; Zemmour D; Kline J; Siwicki M; Garris C; Pucci F; Liao HW; Lin YJ; Newton A; Yaghi OK; Iwamoto Y; Tricot B; Wojtkiewicz GR; Nahrendorf M; Cortez-Retamozo V; Meylan E; Hynes RO; Demay M; Klein A; Bredella MA; Scadden DT; Weissleder R; Pittet MJ
[Ad] Endereço:Center for Systems Biology, Massachusetts General Hospital Research Institute and Harvard Medical School, Boston, MA 02114, USA.
[Ti] Título:Osteoblasts remotely supply lung tumors with cancer-promoting SiglecF neutrophils.
[So] Source:Science;358(6367), 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone marrow-derived myeloid cells can accumulate within tumors and foster cancer outgrowth. Local immune-neoplastic interactions have been intensively investigated, but the contribution of the systemic host environment to tumor growth remains poorly understood. Here, we show in mice and cancer patients ( = 70) that lung adenocarcinomas increase bone stromal activity in the absence of bone metastasis. Animal studies reveal that the cancer-induced bone phenotype involves bone-resident osteocalcin-expressing (Ocn ) osteoblastic cells. These cells promote cancer by remotely supplying a distinct subset of tumor-infiltrating SiglecF neutrophils, which exhibit cancer-promoting properties. Experimentally reducing Ocn cell numbers suppresses the neutrophil response and lung tumor outgrowth. These observations posit osteoblasts as remote regulators of lung cancer and identify SiglecF neutrophils as myeloid cell effectors of the osteoblast-driven protumoral response.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Osso e Ossos/patologia
Lectinas/metabolismo
Neoplasias Pulmonares/patologia
Infiltração de Neutrófilos
Neutrófilos/metabolismo
Neutrófilos/patologia
Osteoblastos/patologia
[Mh] Termos MeSH secundário: Animais
Densidade Óssea
Células da Medula Óssea/patologia
Osso e Ossos/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Células Mieloides/patologia
Neoplasias Experimentais/patologia
Osteocalcina/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Lectins); 0 (Receptor for Advanced Glycation End Products); 0 (SIGLEC5 protein, human); 0 (sRAGE protein, human); 104982-03-8 (Osteocalcin)
[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:171202
[St] Status:MEDLINE


  2 / 5825 MEDLINE  
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[PMID]:29367523
[Au] Autor:Umeda N; Matsumoto I; Sumida T
[Ad] Endereço:Department of Rheumatology, Tsuchiura Kyodo General Hospital.
[Ti] Título:[The pathogenic role of ACPA in rheumatoid arthritis].
[So] Source:Nihon Rinsho Meneki Gakkai Kaishi;40(6):391-395, 2017.
[Is] ISSN:1349-7413
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:  In rheumatoid arthritis (RA), ACPA (anti-citrullinated protein/peptide antibody) is elevated with high specificity, and clinically, anti-CCP (cyclic citrullinated peptide) antibody is widely used for diagnosis of RA. It is thought ACPAs are produced with genetic background such as HLA-DR, environmental factors such as periodontal disease and smoking, however, the pathogenic role of ACPA in RA has not been elucidated. These were showed immune complexes including ACPA or ACPA itself promoted inflammatory cytokine production such as TNF. PADs (peptidylarginine deiminases) were expressed and citrullinated proteins existed in RA synovium. ACPAs were deposited on the site of citrulline in CD68 positive cells of RA synovium. The damage of bone and cartilage is observed in RA. It was also suggested that deposition of ACPAs caused osteoclastogenesis and bone loss. We introduce several findings about the pathogenic role of ACPA in RA.
[Mh] Termos MeSH primário: Anticorpos Anti-Proteína Citrulinada/efeitos adversos
Anticorpos Anti-Proteína Citrulinada/imunologia
Artrite Reumatoide/imunologia
[Mh] Termos MeSH secundário: Antígenos CD
Antígenos de Diferenciação Mielomonocítica
Artrite Reumatoide/diagnóstico
Artrite Reumatoide/metabolismo
Artrite Reumatoide/patologia
Reabsorção Óssea/imunologia
Osso e Ossos/patologia
Cartilagem/patologia
Citrulina/imunologia
Citrulina/metabolismo
Antígenos HLA-DR
Seres Humanos
Mediadores da Inflamação/metabolismo
Osteogênese/imunologia
Doenças Periodontais
Desiminases de Arginina em Proteínas/metabolismo
Fumar
Membrana Sinovial/citologia
Membrana Sinovial/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Citrullinated Protein Antibodies); 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 antigen, human); 0 (HLA-DR Antigens); 0 (Inflammation Mediators); 0 (Tumor Necrosis Factor-alpha); 29VT07BGDA (Citrulline); EC 3.5.3.15 (Protein-Arginine Deiminases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.2177/jsci.40.391


  3 / 5825 MEDLINE  
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[PMID]:28461571
[Au] Autor:Wang M; Fijak M; Hossain H; Markmann M; Nüsing RM; Lochnit G; Hartmann MF; Wudy SA; Zhang L; Gu H; Konrad L; Chakraborty T; Meinhardt A; Bhushan S
[Ad] Endereço:Institute of Anatomy and Cell Biology, Justus-Liebig-University of Giessen, Giessen 35392, Germany.
[Ti] Título:Characterization of the Micro-Environment of the Testis that Shapes the Phenotype and Function of Testicular Macrophages.
[So] Source:J Immunol;198(11):4327-4340, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Macrophages are important in the activation of innate immune responses and in a tissue-specific manner in the maintenance of organ homeostasis. Testicular macrophages (TM), which reside in the testicular interstitial space, comprise the largest leukocyte population in the testes and are assumed to play a relevant function in maintaining testicular immune privilege. Numerous studies have indicated that the interstitial fluid (IF) surrounding the TM has immunosuppressive properties, which may influence the phenotype of TM. However, the identity of the immunosuppressive molecules present in the IF is poorly characterized. We show that the rat testicular IF shifted GM-CSF-induced M1 toward the M2 macrophage phenotype. IF-polarized M2 macrophages mimic the properties of TM, such as increased expression of CD163, high secretion of IL-10, and low secretion of TNF-α. In addition, IF-polarized macrophages display immunoregulatory functions by inducing expansion of immunosuppressive regulatory T cells. We further found that corticosterone was the principal immunosuppressive molecule present in the IF and that the glucocorticoid receptor is needed for induction of the testis-specific phenotype of TM. In addition, TM locally produce small amounts of corticosterone, which suppresses the basal expression of inflammatory genes as a means to render TM refractory to inflammatory stimuli. Taken together, these results suggest that the corticosterone present in the testicular environment shapes the immunosuppressive function and phenotype of TM and that this steroid may play an important role in the establishment and sustenance of the immune privilege of the testis.
[Mh] Termos MeSH primário: Microambiente Celular
Líquido Extracelular/imunologia
Macrófagos/imunologia
Testículo/citologia
Testículo/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Antígenos de Diferenciação Mielomonocítica/genética
Células Cultivadas
Corticosterona/metabolismo
Líquido Extracelular/citologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/farmacologia
Imunidade Inata
Interleucina-10/imunologia
Interleucina-10/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/fisiologia
Masculino
Fenótipo
Ratos
Receptores de Superfície Celular/genética
Testículo/anatomia & histologia
Fator de Necrose Tumoral alfa/imunologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD163 antigen); 0 (Receptors, Cell Surface); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700162


  4 / 5825 MEDLINE  
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[PMID]:28455006
[Au] Autor:Inamoto Y; Martin PJ; Paczesny S; Tabellini L; Momin AA; Mumaw CL; Flowers MED; Lee SJ; Carpenter PA; Storer BE; Hanash S; Hansen JA
[Ad] Endereço:Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, Washington; Department of Hematopoietic Stem Cell Transplantation, National Cancer Center Hospital, Tokyo, Japan. Electronic address: yinamoto@fredhutch.org.
[Ti] Título:Association of Plasma CD163 Concentration with De Novo-Onset Chronic Graft-versus-Host Disease.
[So] Source:Biol Blood Marrow Transplant;23(8):1250-1256, 2017 Aug.
[Is] ISSN:1523-6536
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic graft-versus-host disease (GVHD) is the leading cause of long-term morbidity and mortality after allogeneic hematopoietic cell transplantation. To identify prognostic plasma proteins associated with de novo- or quiescent-onset chronic GVHD (cGVHD), we performed a discovery and validation proteomic study. The total study cohort included 167 consecutive patients who had no clinical evidence of GVHD under minimum glucocorticoid administration and had available plasma samples obtained at 80 ± 14 days after transplantation. We first used high-throughput mass spectrometry to screen pooled plasma using 20 cases with subsequent cGVHD and 20 controls without it, and we identified 20 candidate proteins. We then measured 12 of the 20 candidate proteins by ELISA on the same individual samples and identified 4 proteins for further verification (LGALS3BP, CD5L, CD163, and TXN for de novo onset, and LGALS3BP and CD5L for quiescent onset). The verification cohort included 127 remaining patients. The cumulative incidence of de novo-onset cGVHD was higher in patients with higher plasma soluble CD163 concentrations at day 80 than those with lower concentrations (75% versus 40%, P = .018). The cumulative incidence of de novo- or quiescent-onset cGVHD did not differ statistically according to concentrations of the 3 other proteins at day 80. CD163 is a macrophage scavenger receptor and is elevated in oxidative conditions. These results suggest that monocyte or macrophage activation or increased oxidative stress may contribute to the pathogenesis of cGVHD.
[Mh] Termos MeSH primário: Antígenos CD/sangue
Antígenos de Diferenciação Mielomonocítica/sangue
Doença Enxerto-Hospedeiro/sangue
Transplante de Células-Tronco Hematopoéticas
Receptores de Superfície Celular/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Aloenxertos
Biomarcadores/sangue
Doença Crônica
Feminino
Doença Enxerto-Hospedeiro/epidemiologia
Seres Humanos
Incidência
Ativação de Macrófagos
Macrófagos/metabolismo
Masculino
Meia-Idade
Monócitos/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Biomarkers); 0 (CD163 antigen); 0 (Receptors, Cell Surface)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  5 / 5825 MEDLINE  
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[PMID]:28449029
[Au] Autor:Munz M; Willenborg C; Richter GM; Jockel-Schneider Y; Graetz C; Staufenbiel I; Wellmann J; Berger K; Krone B; Hoffmann P; van der Velde N; Uitterlinden AG; de Groot LCPGM; Sawalha AH; Direskeneli H; Saruhan-Direskeneli G; Guzeldemir-Akcakanat E; Keceli G; Laudes M; Noack B; Teumer A; Holtfreter B; Kocher T; Eickholz P; Meyle J; Doerfer C; Bruckmann C; Lieb W; Franke A; Schreiber S; Nohutcu RM; Erdmann J; Loos BG; Jepsen S; Dommisch H; Schaefer AS
[Ad] Endereço:Department of Periodontology and Synoptic Dentistry, Institute of Dental, Oral and Maxillary Medicine, Charité - University Medicine Berlin, Germany.
[Ti] Título:A genome-wide association study identifies nucleotide variants at SIGLEC5 and DEFA1A3 as risk loci for periodontitis.
[So] Source:Hum Mol Genet;26(13):2577-2588, 2017 07 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. The disease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory response to a dysbiotic oral microbiome. Previous genome-wide association studies (GWAS) have reported several suggestive susceptibility loci. Here, we conducted a GWAS using a German and Dutch case-control sample of aggressive periodontitis (AgP, 896 cases, 7,104 controls), a rare but highly severe and early-onset form of periodontitis, validated the associations in a German sample of severe forms of the more moderate phenotype chronic periodontitis (CP) (993 cases, 1,419 controls). Positive findings were replicated in a Turkish sample of AgP (223 cases, 564 controls). A locus at SIGLEC5 (sialic acid binding Ig-like lectin 5) and a chromosomal region downstream of the DEFA1A3 locus (defensin alpha 1-3) showed association with both disease phenotypes and were associated with periodontitis at a genome-wide significance level in the pooled samples, with P = 1.09E-08 (rs4284742,-G; OR = 1.34, 95% CI = 1.21-1.48) and P = 5.48E-10 (rs2738058,-T; OR = 1.28, 95% CI = 1.18-1.38), respectively. SIGLEC5 is expressed in various myeloid immune cells and classified as an inhibitory receptor with the potential to mediate tyrosine phosphatases SHP-1/-2 dependent signaling. Alpha defensins are antimicrobial peptides with expression in neutrophils and mucosal surfaces and a role in phagocyte-mediated host defense. This study identifies the first shared genetic risk loci of AgP and CP with genome-wide significance and highlights the role of innate and adaptive immunity in the etiology of periodontitis.
[Mh] Termos MeSH primário: Antígenos CD/genética
Antígenos de Diferenciação Mielomonocítica/genética
Periodontite Crônica/genética
Lectinas/genética
Peptídeos Cíclicos/genética
alfa-Defensinas/genética
[Mh] Termos MeSH secundário: Adulto
Periodontite Agressiva/genética
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Estudos de Casos e Controles
Feminino
Loci Gênicos
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Genótipo
Seres Humanos
Lectinas/metabolismo
Masculino
Meia-Idade
Nucleotídeos
Peptídeos Cíclicos/metabolismo
Fenótipo
Polimorfismo de Nucleotídeo Único/genética
Fatores de Risco
Turquia
alfa-Defensinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (DEFA1A3 protein, human); 0 (Lectins); 0 (Nucleotides); 0 (Peptides, Cyclic); 0 (SIGLEC5 protein, human); 0 (alpha-Defensins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx151


  6 / 5825 MEDLINE  
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[PMID]:29220404
[Au] Autor:Rumney RMH; Coffelt SB; Neale TA; Dhayade S; Tozer GM; Miller G
[Ad] Endereço:Department of Oncology and Metabolism, University of Sheffield, Sheffield, United Kingdom.
[Ti] Título:PyMT-Maclow: A novel, inducible, murine model for determining the role of CD68 positive cells in breast tumor development.
[So] Source:PLoS One;12(12):e0188591, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD68+ tumor-associated macrophages (TAMs) are pro-tumorigenic, pro-angiogenic and are associated with decreased survival rates in patients with cancer, including breast cancer. Non-specific models of macrophage ablation reduce the number of TAMs and limit the development of mammary tumors. However, the lack of specificity and side effects associated with these models compromise their reliability. We hypothesized that specific and controlled macrophage depletion would provide precise data on the effects of reducing TAM numbers on tumor development. In this study, the MacLow mouse model of doxycycline-inducible and selective CD68+ macrophage depletion was crossed with the murine mammary tumor virus (MMTV)-Polyoma virus middle T antigen (PyMT) mouse model of spontaneous ductal breast adenocarcinoma to generate the PyMT-MacLow line. In doxycycline-treated PyMT-MacLow mice, macrophage numbers were decreased in areas surrounding tumors by 43%. Reducing the number of macrophages by this level delayed tumor progression, generated less proliferative tumors, decreased the vascularization of carcinomas and down-regulated the expression of many pro-angiogenic genes. These results demonstrate that depleting CD68+ macrophages in an inducible and selective manner delays the development of mammary tumors and that the PyMT-MacLow model is a useful and unique tool for studying the role of TAMs in breast cancer.
[Mh] Termos MeSH primário: Antígenos CD/imunologia
Antígenos de Diferenciação Mielomonocítica/imunologia
Neoplasias da Mama/imunologia
Modelos Animais de Doenças
Macrófagos/imunologia
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Doxiciclina/farmacologia
Feminino
Seres Humanos
Macrófagos/efeitos dos fármacos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD68 antigen, human); N12000U13O (Doxycycline)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188591


  7 / 5825 MEDLINE  
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[PMID]:27770812
[Au] Autor:Doeschl-Wilson A; Wilson A; Nielsen J; Nauwynck H; Archibald A; Ait-Ali T
[Ad] Endereço:The Roslin Institute & R(D)SVS, University of Edinburgh, Easter Bush, Edinburgh, UK. Andrea.Wilson@roslin.ed.ac.uk.
[Ti] Título:Combining laboratory and mathematical models to infer mechanisms underlying kinetic changes in macrophage susceptibility to an RNA virus.
[So] Source:BMC Syst Biol;10(1):101, 2016 10 22.
[Is] ISSN:1752-0509
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Macrophages are essential to innate immunity against many pathogens, but some pathogens also target macrophages as routes to infection. The Porcine Reproductive and Respiratory Syndrome virus (PRRSV) is an RNA virus that infects porcine alveolar macrophages (PAMs) causing devastating impact on global pig production. Identifying the cellular mechanisms that mediate PAM susceptibility to the virus is crucial for developing effective interventions. Previous evidence suggests that the scavenger receptor CD163 is essential for productive infection of PAMs with PRRSV. Here we use an integrative in-vitro-in-silico modelling approach to determine whether and how PAM susceptibility to PRRSV changes over time, to assess the role of CD163 expression on such changes, and to infer other potential causative mechanisms altering cell susceptibility. RESULTS: Our in-vitro experiment showed that PAM susceptibility to PRRSV changed considerably over incubation time. Moreover, an increasing proportion of PAMs apparently lacking CD163 were found susceptible to PRRSV at the later incubation stages, thus conflicting with current understanding that CD163 is essential for productive infection of PAMs with PRRSV. We developed process based dynamic mathematical models and fitted these to the data to assess alternative hypotheses regarding potential underlying mechanisms for the observed susceptibility and biomarker trends. The models informed by our data support the hypothesis that although CD163 may have enhanced cell susceptibility, it was not essential for productive infection in our study. Instead the models promote the existence of a reversible cellular state, such as macrophage polarization, mediated in a density dependent manner by autocrine factors, to be responsible for the observed kinetics in cell susceptibility. CONCLUSIONS: Our dynamic model-inference approach provides strong support that PAM susceptibility to the PRRS virus is transient, reversible and can be mediated by compounds produced by the target cells themselves, and that these can render PAMs lacking the CD163 receptor susceptible to PRRSV. The results have implications for the development of therapeutics aiming to boost target cell resistance and prompt future investigation of dynamic changes in macrophage susceptibility to PRRSV and other viruses.
[Mh] Termos MeSH primário: Laboratórios
Macrófagos/virologia
Modelos Biológicos
Vírus da Síndrome Respiratória e Reprodutiva Suína/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Regulação da Expressão Gênica
Cinética
Macrófagos/metabolismo
Receptores de Superfície Celular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD163 antigen); 0 (Receptors, Cell Surface)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171223
[Lr] Data última revisão:
171223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  8 / 5825 MEDLINE  
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[PMID]:27777207
[Au] Autor:Zhong SM; Qin YH; Li ZC; Wei YS
[Ad] Endereço:Department of Laboratory Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, China. E-mail: shimaozhong_edu@sina.com.
[Ti] Título:[Clinical value of detecting serum soluble CD163 level in patients with atrial fibrillation].
[So] Source:Nan Fang Yi Ke Da Xue Xue Bao;36(10):1406-1409, 2016 Oct 20.
[Is] ISSN:1673-4254
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the relationship between atrial fibrillation (AF) and serum soluble CD163. METHODS: A total of 336 patients with heart valve disease were included in this study, including 167 with AF and 169 with sinus rhythm. The clinical data were compared between the two grops, and Logistic regression analysis was used to identify the risk factors associated with AF. RESULTS: The levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), tumor necrosis factor (TNF), interleukin-6 (IL - 6), high-sensitivity C-reactive protein (hs-CRP) and left atrial diameter (LAD) all differed significantly between the two groups (P<0.05). Serum soluble CD163 levels in AF patients were significantly higher than those in patients with sinus rhythm (P<0.05). Serum soluble CD163 was positively correlated with TNF (r=0.244, P=0.244), IL-6 (r=0.186, P=0.186), hs-CRP (r=0.183, P=0.183) and LAD (r=0.194, P=0.194) in patients with AF. Logistic regression analysis showed that LAD, IL-6, TNF, hs-CRP and CD163 were all associated with AF. ROC curve analysis showed that the area under curve of serum soluble CD163 was 0.861 in patients with AF (CI 95%: 0.820-0.901, P<0.01) with a sensitivity and a specificity of 80.8 and 76.9%, respectively. CONCLUSION: Serum soluble CD163 level may be a risk factor for AF, and an increased soluble CD163 level may indicate active inflammation in AF patients.
[Mh] Termos MeSH primário: Antígenos CD/sangue
Antígenos de Diferenciação Mielomonocítica/sangue
Fibrilação Atrial/sangue
Inflamação/sangue
Receptores de Superfície Celular/sangue
[Mh] Termos MeSH secundário: Proteína C-Reativa/análise
Átrios do Coração/patologia
Seres Humanos
Interleucina-6/sangue
Lipoproteínas HDL/sangue
Lipoproteínas LDL/sangue
Fatores de Risco
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD163 antigen); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Lipoproteins, HDL); 0 (Lipoproteins, LDL); 0 (Receptors, Cell Surface); 0 (Tumor Necrosis Factor-alpha); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  9 / 5825 MEDLINE  
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[PMID]:27777198
[Au] Autor:Wang LY; Yi JH; Xu HC; Wu XF; Li DY; Han J
[Ad] Endereço:Department of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China. E-mail: wly10384938@163.com.
[Ti] Título:[Effect of low-selenium diet on expressions of CCR7, CD206 and CD163 in the liver and kidney of rats].
[So] Source:Nan Fang Yi Ke Da Xue Xue Bao;36(10):1357-1363, 2016 Oct 20.
[Is] ISSN:1673-4254
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate the effect of low-selenium diet on the liver and kidneys of rats and explore the role of macrophage polarization into M1 and M2 phenotypes in liver and kidney injuries. METHODS: Twenty-four rats (12 female and 12 male) were randomly divided into control group and low-selenium group and fed with normal chow (dietary selenium of 0.18 mg/kg) and low-selenium diet (dietary selenium of 0.02 mg/kg) for 109 days. After the feeding, the rats were sacrificed for HE staining to observe liver and kidney pathologies, and immunohistochemistry was performed for analyzing CCR7, CD206, CD163-positive cell numbers in the liver and kidneys. RESULTS: The rats in low-selenium group showed severer fibrosis in the liver and kidney than the control group. In either male or female rats in low-selenium group, CCR7 and CD206 expressions in the liver were comparable with those in control group, but CD163 expression was lower than that in the control group (P<0.05 for both female and male rats). In the kidney, the proximal tubule showed a slightly higher while the distal tubule showed a slightly lower CCR7 expression in low selenium group than in the control group (P>0.05). In low-selenium group, a significantly lower CD163 expression in the distal tubule and a significantly higher CD206 expression in the proximal tubule were noted as compared with the control group (P<0.05 in both female and male rats). Compared with the control rats, the male rats in low-selenium group, but not the female rats, showed a significantly lower CD163 expression in the proximal tubule of the kidney (P<0.05); the female but not the male rats in low-selenium group show a higher CD206 expression in the distal tubule (P<0.05). CONCLUSION: Low-selenium diet can cause liver and kidney fibrosis in rats and may inhibit macrophage activation into the M2 phenotype.
[Mh] Termos MeSH primário: Dieta
Rim/metabolismo
Fígado/metabolismo
Ativação de Macrófagos
Selênio/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Feminino
Fibrose
Rim/patologia
Lectinas Tipo C/metabolismo
Fígado/patologia
Masculino
Lectinas de Ligação a Manose/metabolismo
Ratos
Receptores CCR7/metabolismo
Receptores de Superfície Celular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD163 antigen); 0 (Ccr7 protein, rat); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (Receptors, CCR7); 0 (Receptors, Cell Surface); 0 (mannose receptor); H6241UJ22B (Selenium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29073216
[Au] Autor:Motwani MP; Newson J; Kwong S; Richard-Loendt A; Colas R; Dalli J; Gilroy DW
[Ad] Endereço:Centre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, United Kingdom.
[Ti] Título:Prolonged immune alteration following resolution of acute inflammation in humans.
[So] Source:PLoS One;12(10):e0186964, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute inflammation is an immediate response to infection and injury characterised by the influx of granulocytes followed by phagocytosing mononuclear phagocytes. Provided the antigen is cleared and the immune system of the host is fully functional, the acute inflammatory response will resolve. Until now it is considered that resolution then leads back to homeostasis, the physiological state tissues experienced before inflammation occurred. Using a human model of acute inflammation driven by intradermal UV killed Escherichia coli, we found that bacteria and granulocyte clearance as well as pro-inflammatory cytokine catabolism occurred by 72h. However, following a lag phase of about 4 days there was an increase in numbers of memory T cells and CD163+ macrophage at the post-resolution site up to day 17 as well as increased biosynthesis of cyclooxygenase-derived prostanoids and DHA-derived D series resolvins. Inhibiting post-resolution prostanoids using naproxen showed that numbers of tissue memory CD4 cells were under the endogenous control of PGE2, which exerts its suppressive effects on T cell proliferation via the EP4 receptor. In addition, we re-challenged the post-resolution site with a second injection of E. coli, which when compared to saline controls resulted in primarily a macrophage-driven response with comparatively fewer PMNs; the macrophage-dominated response was reversed by cyclooxygenase inhibition. Re-challenge experiments were also carried out in mice where we obtained similar results as in humans. Therefore, we report that acute inflammatory responses in both humans and rodents do not revert back to homeostasis, but trigger a hitherto unappreciated sequence of immunological events that dictate subsequent immune response to infection.
[Mh] Termos MeSH primário: Inflamação/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Animais
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Contagem de Células
Proliferação Celular/efeitos dos fármacos
Dinoprostona/farmacologia
Escherichia coli/efeitos dos fármacos
Escherichia coli/fisiologia
Escherichia coli/efeitos da radiação
Feminino
Seres Humanos
Inflamação/microbiologia
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos/metabolismo
Masculino
Camundongos
Viabilidade Microbiana/efeitos da radiação
Meia-Idade
Receptores de Superfície Celular/metabolismo
Linfócitos T/citologia
Linfócitos T/efeitos dos fármacos
Linfócitos T/imunologia
Raios Ultravioleta
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD163 antigen); 0 (Receptors, Cell Surface); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171027
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186964



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