Base de dados : MEDLINE
Pesquisa : D12.644.276.374.200.120 [Categoria DeCS]
Referências encontradas : 5219 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 522 ir para página                         

  1 / 5219 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29182510
[Au] Autor:Soe HJ; Khan AM; Manikam R; Samudi Raju C; Vanhoutte P; Sekaran SD
[Ad] Endereço:1​Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
[Ti] Título:High dengue virus load differentially modulates human microvascular endothelial barrier function during early infection.
[So] Source:J Gen Virol;98(12):2993-3007, 2017 Dec.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Plasma leakage is the main pathophysiological feature in severe dengue, resulting from altered vascular barrier function associated with an inappropriate immune response triggered upon infection. The present study investigated functional changes using an electric cell-substrate impedance sensing system in four (brain, dermal, pulmonary and retinal) human microvascular endothelial cell (MEC) lines infected with purified dengue virus, followed by assessment of cytokine profiles and the expression of inter-endothelial junctional proteins. Modelling of changes in electrical impedance suggests that vascular leakage in dengue-infected MECs is mostly due to the modulation of cell-to-cell interactions, while this loss of vascular barrier function observed in the infected MECs varied between cell lines and DENV serotypes. High levels of inflammatory cytokines (IL-6 and TNF-α), chemokines (CXCL1, CXCL5, CXCL11, CX3CL1, CCL2 and CCL20) and adhesion molecules (VCAM-1) were differentially produced in the four infected MECs. Further, the tight junctional protein, ZO-1, was down-regulated in both the DENV-1-infected brain and pulmonary MECs, while claudin-1, PECAM-1 and VE-cadherin were differentially expressed in these two MECs after infection. Non-purified virus stock was also studied to investigate the impact of virus stock purity on dengue-specific immune responses, and the results suggest that virus stock propagated through cell culture may include factors that mask or alter the DENV-specific immune responses of the MECs. The findings of the present study show that high DENV load differentially modulates human microvascular endothelial barrier function and disrupts the function of inter-endothelial junctional proteins during early infection with organ-specific cytokine production.
[Mh] Termos MeSH primário: Células Endoteliais/virologia
Endotélio Vascular/virologia
Interações Hospedeiro-Patógeno
Carga Viral/imunologia
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antígenos CD/imunologia
Encéfalo/citologia
Encéfalo/imunologia
Encéfalo/virologia
Caderinas/genética
Caderinas/imunologia
Linhagem Celular
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Quimiocina CCL20/genética
Quimiocina CCL20/imunologia
Quimiocina CX3CL1/genética
Quimiocina CX3CL1/imunologia
Quimiocinas CXC/genética
Quimiocinas CXC/imunologia
Claudina-1/genética
Claudina-1/imunologia
Vírus da Dengue/genética
Vírus da Dengue/crescimento & desenvolvimento
Vírus da Dengue/imunologia
Derme/citologia
Derme/imunologia
Derme/virologia
Impedância Elétrica
Células Endoteliais/citologia
Células Endoteliais/imunologia
Endotélio Vascular/citologia
Endotélio Vascular/imunologia
Regulação da Expressão Gênica
Seres Humanos
Interleucina-6/genética
Interleucina-6/imunologia
Pulmão/citologia
Pulmão/imunologia
Pulmão/virologia
Especificidade de Órgãos
Permeabilidade
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/imunologia
Retina/citologia
Retina/imunologia
Retina/virologia
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
Molécula 1 de Adesão de Célula Vascular/genética
Molécula 1 de Adesão de Célula Vascular/imunologia
Internalização do Vírus
Proteína da Zônula de Oclusão-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CCL2 protein, human); 0 (CCL20 protein, human); 0 (CX3CL1 protein, human); 0 (Cadherins); 0 (Chemokine CCL2); 0 (Chemokine CCL20); 0 (Chemokine CX3CL1); 0 (Chemokines, CXC); 0 (Claudin-1); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (TJP1 protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 0 (Zonula Occludens-1 Protein); 0 (cadherin 5)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171213
[Lr] Data última revisão:
171213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000981


  2 / 5219 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28409836
[Au] Autor:Wang Y; Zhang S; Luo L; Norström E; Braun OÖ; Mörgelin M; Thorlacius H
[Ad] Endereço:Department of Clinical Sciences, Section for Surgery, Lund University, Malmö, Sweden.
[Ti] Título:Platelet-derived microparticles regulates thrombin generation via phophatidylserine in abdominal sepsis.
[So] Source:J Cell Physiol;233(2):1051-1060, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis is associated with dysfunctional coagulation. Recent data suggest that platelets play a role in sepsis by promoting neutrophil accumulation. Herein, we show that cecal ligation and puncture (CLP) triggered systemic inflammation, which is characterized by formation of IL-6 and CXC chemokines as well as neutrophil accumulation in the lung. Platelet depletion decreased neutrophil accumulation, IL-6, and CXC chemokines formation in septic lungs. Depletion of platelets increased peak thrombin formation and total thrombin generation (TG) in plasma from septic animals. CLP elevated circulating levels of platelet-derived microparticles (PMPs). In vitro generated PMPs were a potent inducer of TG. Interestingly, in vitro wild-type recombinant annexin V abolished PMP-induced thrombin formation whereas a mutant annexin V protein, which does not bind to phosphatidylserine (PS), had no effect. Administration of wild-type, but not mutant annexin V, significantly inhibited thrombin formation in septic animals. Moreover, CLP-induced formation of thrombin-antithrombin complexes were reduced in platelet-depleted mice and in animals pretreated with annexin V. PMP-induced TG attenuated in FXII- and FVII-deficient plasma. These findings suggest that sepsis-induced TG is dependent on platelets. Moreover, PMPs formed in sepsis are a potent inducer of TG via PS exposure, and activation of both the intrinsic and extrinsic pathway of coagulation. In conclusion, these observations suggest that PMPs and PS play an important role in dysfunctional coagulation in abdominal sepsis.
[Mh] Termos MeSH primário: Coagulação Sanguínea
Plaquetas/metabolismo
Micropartículas Derivadas de Células/metabolismo
Fosfatidilserinas/sangue
Sepse/sangue
Trombina/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A5/sangue
Antitrombina III
Plaquetas/imunologia
Plaquetas/microbiologia
Plaquetas/ultraestrutura
Micropartículas Derivadas de Células/imunologia
Micropartículas Derivadas de Células/microbiologia
Micropartículas Derivadas de Células/ultraestrutura
Quimiocinas CXC/metabolismo
Modelos Animais de Doenças
Inflamação/sangue
Inflamação/imunologia
Inflamação/microbiologia
Interleucina-6/metabolismo
Pulmão/imunologia
Pulmão/metabolismo
Pulmão/microbiologia
Masculino
Camundongos Endogâmicos C57BL
Infiltração de Neutrófilos
Peptídeo Hidrolases/sangue
Sepse/imunologia
Sepse/microbiologia
Sepse/patologia
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A5); 0 (Chemokines, CXC); 0 (Interleukin-6); 0 (Phosphatidylserines); 0 (antithrombin III-protease complex); 0 (interleukin-6, mouse); 9000-94-6 (Antithrombin III); EC 3.4.- (Peptide Hydrolases); EC 3.4.21.5 (Thrombin)
[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:170415
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25959


  3 / 5219 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28874445
[Au] Autor:Villegas-Mendez A; Strangward P; Shaw TN; Rajkovic I; Tosevski V; Forman R; Muller W; Couper KN
[Ad] Endereço:Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom ana.villegas-mendez@manchester.ac.uk kevin.couper@manchester.ac.uk.
[Ti] Título:Gamma Interferon Mediates Experimental Cerebral Malaria by Signaling within Both the Hematopoietic and Nonhematopoietic Compartments.
[So] Source:Infect Immun;85(11), 2017 Nov.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Experimental cerebral malaria (ECM) is a gamma interferon (IFN-γ)-dependent syndrome. However, whether IFN-γ promotes ECM through direct and synergistic targeting of multiple cell populations or by acting primarily on a specific responsive cell type is currently unknown. Here, using a panel of cell- and compartment-specific IFN-γ receptor 2 (IFN-γR2)-deficient mice, we show that IFN-γ causes ECM by signaling within both the hematopoietic and nonhematopoietic compartments. Mechanistically, hematopoietic and nonhematopoietic compartment-specific IFN-γR signaling exerts additive effects in orchestrating intracerebral inflammation, leading to the development of ECM. Surprisingly, mice with specific deletion of IFN-γR2 expression on myeloid cells, T cells, or neurons were completely susceptible to terminal ECM. Utilizing a reductionist system, we show that synergistic IFN-γ and tumor necrosis factor (TNF) stimulation promotes strong activation of brain blood vessel endothelial cells. Combined, our data show that within the hematopoietic compartment, IFN-γ causes ECM by acting redundantly or by targeting non-T cell or non-myeloid cell populations. Within the nonhematopoietic compartment, brain endothelial cells, but not neurons, may be the major target of IFN-γ leading to ECM development. Collectively, our data provide information on how IFN-γ mediates the development of cerebral pathology during malaria infection.
[Mh] Termos MeSH primário: Encéfalo/imunologia
Células Endoteliais/imunologia
Interferon gama/genética
Malária Cerebral/genética
Plasmodium berghei/patogenicidade
Receptores de Interferon/genética
[Mh] Termos MeSH secundário: Animais
Encéfalo/irrigação sanguínea
Encéfalo/parasitologia
Encéfalo/patologia
Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/imunologia
Quimiocinas CXC/genética
Quimiocinas CXC/imunologia
Modelos Animais de Doenças
Células Endoteliais/parasitologia
Regulação da Expressão Gênica
Interferon gama/imunologia
Interleucinas/genética
Interleucinas/imunologia
Malária Cerebral/imunologia
Malária Cerebral/patologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Mieloides/imunologia
Células Mieloides/parasitologia
Neurônios/imunologia
Neurônios/parasitologia
Plasmodium berghei/imunologia
Receptores de Interferon/deficiência
Receptores de Interferon/imunologia
Transdução de Sinais
Linfócitos T/imunologia
Linfócitos T/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Chemokines, CXC); 0 (Ifngr2 protein, mouse); 0 (Interleukins); 0 (Receptors, Interferon); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE


  4 / 5219 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28866083
[Au] Autor:Zhang L; Liu X; Liu J; Ma L; Zhou Z; Song Y; Cao B
[Ad] Endereço:College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, PR China.
[Ti] Título:The developmental transcriptome landscape of receptive endometrium during embryo implantation in dairy goats.
[So] Source:Gene;633:82-95, 2017 Oct 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Under natural conditions, some embryos cannot implant successfully because of the dysfunction of receptive endometrium (RE). Thus, it is imperative for us to study the molecular mechanisms involved in the formation of the RE from pre-receptive endometrium (PE). In this study, the endometrium from gestational day 5 (D5, PE) and gestational day 15 (D15, RE) dairy goats were selected to systematically analyze the transcriptome using strand-specific Ribo-Zero RNA-Seq, >120 million high-quality paired-end reads were generated and 47,616 transcripts were identified in the endometrium of dairy goats. A total of 810 mRNAs were differentially expressed genes (DEGs) between the RE and PE meeting the criteria of P-values<0.05. Bioinformatics analysis of the DEGs revealed that a number of biological processes and pathways were potentially involved in the establishment of the RE, notably energy metabolism and amino acid metabolism. Furthermore, we speculated that CXCL14, IGFBP3, and LGALS15 potentially participated in the development of endometrium. What's more, putative SNPs, InDels and AS events were identified and analyzed in the endometrium. In a word, this resulting view of the transcriptome greatly enhances the comprehensive transcript catalog and uncovers the global trends in gene expression during the formation of receptive endometrium in dairy goats.
[Mh] Termos MeSH primário: Implantação do Embrião/genética
Endométrio/metabolismo
Cabras/embriologia
Cabras/genética
Transcriptoma
[Mh] Termos MeSH secundário: Animais
Quimiocinas CXC/genética
Feminino
Galectinas/genética
Perfilação da Expressão Gênica
Idade Gestacional
Mutação INDEL
Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
Polimorfismo de Nucleotídeo Único
RNA Mensageiro/metabolismo
Análise de Sequência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines, CXC); 0 (Galectins); 0 (Insulin-Like Growth Factor Binding Protein 3); 0 (RNA, Messenger)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170904
[St] Status:MEDLINE


  5 / 5219 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28842479
[Au] Autor:Johnson ZI; Doolittle AC; Snuggs JW; Shapiro IM; Le Maitre CL; Risbud MV
[Ad] Endereço:From the Department of Orthopaedic Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 and.
[Ti] Título:TNF-α promotes nuclear enrichment of the transcription factor TonEBP/NFAT5 to selectively control inflammatory but not osmoregulatory responses in nucleus pulposus cells.
[So] Source:J Biol Chem;292(42):17561-17575, 2017 Oct 20.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intervertebral disc degeneration (IDD) causes chronic back pain and is linked to production of proinflammatory molecules by nucleus pulposus (NP) and other disc cells. Activation of tonicity-responsive enhancer-binding protein (TonEBP)/NFAT5 by non-osmotic stimuli, including proinflammatory molecules, occurs in cells involved in immune response. However, whether inflammatory stimuli activate TonEBP in NP cells and whether TonEBP controls inflammation during IDD is unknown. We show that TNF-α, but not IL-1ß or LPS, promoted nuclear enrichment of TonEBP protein. However, TNF-α-mediated activation of TonEBP did not cause induction of osmoregulatory genes. RNA sequencing showed that 8.5% of TNF-α transcriptional responses were TonEBP-dependent and identified genes regulated by both TNF-α and TonEBP. These genes were over-enriched in pathways and diseases related to inflammatory response and inhibition of matrix metalloproteases. Based on RNA-sequencing results, we further investigated regulation of novel TonEBP targets , , and TonEBP acted synergistically with TNF-α and LPS to induce -proximal promoter activity. Interestingly, this regulation required a highly conserved NF-κB-binding site but not a predicted TonE, suggesting cross-talk between these two members of the Rel family. Finally, analysis of human NP tissue showed that expression correlated with canonical osmoregulatory targets , , and , supporting findings that the inflammatory milieu during IDD does not interfere with TonEBP osmoregulation. In summary, whereas TonEBP participates in the proinflammatory response to TNF-α, therapeutic strategies targeting this transcription factor for treatment of disc disease must spare osmoprotective, prosurvival, and matrix homeostatic activities.
[Mh] Termos MeSH primário: Disco Intervertebral/metabolismo
Osmorregulação
Fatores de Transcrição/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Aldeído Redutase/biossíntese
Aldeído Redutase/genética
Animais
Linhagem Celular
Quimiocinas CXC/biossíntese
Quimiocinas CXC/genética
Criança
Pré-Escolar
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas de Choque Térmico/biossíntese
Proteínas de Choque Térmico/genética
Seres Humanos
Lactente
Inflamação/genética
Inflamação/metabolismo
Inflamação/patologia
Disco Intervertebral/patologia
Degeneração do Disco Intervertebral/genética
Degeneração do Disco Intervertebral/metabolismo
Degeneração do Disco Intervertebral/patologia
Lipopolissacarídeos/toxicidade
Masculino
Glicoproteínas de Membrana/biossíntese
Glicoproteínas de Membrana/genética
Proteínas de Membrana Transportadoras/biossíntese
Proteínas de Membrana Transportadoras/genética
Meia-Idade
Ratos
Simportadores/biossíntese
Simportadores/genética
Fatores de Transcrição/genética
Fator de Necrose Tumoral alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines, CXC); 0 (Heat-Shock Proteins); 0 (Lipopolysaccharides); 0 (Membrane Glycoproteins); 0 (Membrane Transport Proteins); 0 (NFAT5 protein, human); 0 (Nfat5 protein, rat); 0 (Symporters); 0 (Transcription Factors); 0 (Tumor Necrosis Factor-alpha); 146890-04-2 (SLC5A3 protein, human); 148686-53-7 (taurine transporter); EC 1.1.1.21 (AKR1B1 protein, human); EC 1.1.1.21 (Akr1b1 protein, rat); EC 1.1.1.21 (Aldehyde Reductase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170827
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.790378


  6 / 5219 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28759013
[Au] Autor:Krawczyk KM; Nilsson H; Allaoui R; Lindgren D; Arvidsson M; Leandersson K; Johansson ME
[Ad] Endereço:Department of Translational Medicine, Center for Molecular Pathology, Lund University, Malmö, Sweden.
[Ti] Título:Papillary renal cell carcinoma-derived chemerin, IL-8, and CXCL16 promote monocyte recruitment and differentiation into foam-cell macrophages.
[So] Source:Lab Invest;97(11):1296-1305, 2017 Nov.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Papillary renal cell carcinoma (pRCC) is the second most common type of renal cell carcinoma. The only curative treatment available for pRCC is radical surgery. If the disease becomes widespread, neither chemo- nor radiotherapy will have therapeutic effect, hence further research on pRCC is of utmost importance. Histologically, pRCC is characterized by a papillary growth pattern with focal aggregation of macrophages of the foam cell phenotype. In other forms of cancer, a clear role for tumor-associated macrophages during cancer growth and progression has been shown. Although the presence of foamy macrophages is a histological hallmark of pRCC tumors, little is known regarding their role in pRCC biology. In order to study the interaction between pRCC tumor and myeloid cells, we established primary cultures from pRCC tissue. We show that human pRCC cells secrete the chemokines IL-8, CXCL16, and chemerin, and that these factors attract primary human monocytes in vitro. RNAseq data from The Cancer Genome Atlas confirmed a high expression of these factors in pRCC tissue. Conditioned medium from pRCC cultures induced a shift in human monocytes toward the M2 macrophage phenotype. In extended cultures, these macrophages became enlarged and loaded with lipids, adopting the foam cell morphology found in pRCC tissue. These results show for the first time that pRCC primary tumor cells secrete factors that attract and differentiate monocytes into anti-inflammatory tumor-associated macrophages with foam cell histology.
[Mh] Termos MeSH primário: Carcinoma de Células Renais/metabolismo
Quimiocinas CXC/metabolismo
Quimiocinas/metabolismo
Células Espumosas/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Interleucina-8/metabolismo
Neoplasias Renais/metabolismo
Monócitos/metabolismo
Receptores Depuradores/metabolismo
[Mh] Termos MeSH secundário: Idoso
Carcinoma de Células Renais/imunologia
Carcinoma de Células Renais/patologia
Carcinoma de Células Renais/cirurgia
Transdiferenciação Celular
Células Cultivadas
Quimiocina CXCL16
Quimiocinas/secreção
Quimiocinas CXC/secreção
Quimiotaxia de Leucócito
Técnicas de Cocultura
Meios de Cultivo Condicionados
Células Espumosas/imunologia
Células Espumosas/patologia
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/secreção
Interleucina-8/secreção
Neoplasias Renais/imunologia
Neoplasias Renais/patologia
Neoplasias Renais/secreção
Masculino
Meia-Idade
Monócitos/imunologia
Monócitos/patologia
Gradação de Tumores
Proteínas de Neoplasias/metabolismo
Proteínas de Neoplasias/secreção
Nefrectomia
Carga Tumoral
Células Tumorais Cultivadas
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL16 protein, human); 0 (Chemokine CXCL16); 0 (Chemokines); 0 (Chemokines, CXC); 0 (Culture Media, Conditioned); 0 (IL8 protein, human); 0 (Intercellular Signaling Peptides and Proteins); 0 (Interleukin-8); 0 (Neoplasm Proteins); 0 (Receptors, Scavenger); 0 (chemerin protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2017.78


  7 / 5219 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28600292
[Au] Autor:Reyat JS; Chimen M; Noy PJ; Szyroka J; Rainger GE; Tomlinson MG
[Ad] Endereço:School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Birmingham B15 2TT, United Kingdom; and.
[Ti] Título:ADAM10-Interacting Tetraspanins Tspan5 and Tspan17 Regulate VE-Cadherin Expression and Promote T Lymphocyte Transmigration.
[So] Source:J Immunol;199(2):666-676, 2017 Jul 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The recruitment of blood leukocytes across the endothelium to sites of tissue infection is central to inflammation, but also promotes chronic inflammatory diseases. A disintegrin and metalloproteinase 10 (ADAM10) is a ubiquitous transmembrane molecular scissor that is implicated in leukocyte transmigration by proteolytically cleaving its endothelial substrates. These include VE-cadherin, a homotypic adhesion molecule that regulates endothelial barrier function, and transmembrane chemokines CX3CL1 and CXCL16, which have receptors on leukocytes. However, a definitive role for endothelial ADAM10 in transmigration of freshly isolated primary leukocytes under flow has not been demonstrated, and the relative importance of distinct ADAM10 substrates is unknown. Emerging evidence suggests that ADAM10 can be regarded as six different molecular scissors with different substrate specificities, depending on which of six TspanC8 tetraspanins it is associated with, but TspanC8s remain unstudied in leukocyte transmigration. In the current study, ADAM10 knockdown on primary HUVECs was found to impair transmigration of freshly isolated human peripheral blood T lymphocytes, but not neutrophils or B lymphocytes, in an in vitro flow assay. This impairment was due to delayed transmigration rather than a complete block, and was overcome in the presence of neutrophils. Transmigration of purified lymphocytes was dependent on ADAM10 regulation of VE-cadherin, but not CX3CL1 and CXCL16. Tspan5 and Tspan17, the two most closely related TspanC8s by sequence, were the only TspanC8s that regulated VE-cadherin expression and were required for lymphocyte transmigration. Therefore endothelial Tspan5- and Tspan17-ADAM10 complexes may regulate inflammation by maintaining normal VE-cadherin expression and promoting T lymphocyte transmigration.
[Mh] Termos MeSH primário: Proteína ADAM10/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Antígenos CD/genética
Caderinas/genética
Proteínas de Membrana/metabolismo
Linfócitos T/fisiologia
Tetraspaninas/metabolismo
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Proteína ADAM10/deficiência
Proteína ADAM10/genética
Proteína ADAM10/imunologia
Secretases da Proteína Precursora do Amiloide/deficiência
Secretases da Proteína Precursora do Amiloide/genética
Secretases da Proteína Precursora do Amiloide/imunologia
Antígenos CD/metabolismo
Linfócitos B/imunologia
Linfócitos B/fisiologia
Caderinas/metabolismo
Células Cultivadas
Quimiocina CX3CL1/genética
Quimiocina CX3CL1/imunologia
Quimiocina CXCL16
Quimiocinas CXC/genética
Quimiocinas CXC/imunologia
Células Endoteliais/imunologia
Células Endoteliais/fisiologia
Seres Humanos
Inflamação/imunologia
Proteínas de Membrana/deficiência
Proteínas de Membrana/genética
Proteínas de Membrana/imunologia
Neutrófilos/imunologia
Neutrófilos/fisiologia
Receptores Depuradores/genética
Receptores Depuradores/imunologia
Linfócitos T/imunologia
Tetraspaninas/genética
Tetraspaninas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CX3CL1 protein, human); 0 (CXCL16 protein, human); 0 (Cadherins); 0 (Chemokine CX3CL1); 0 (Chemokine CXCL16); 0 (Chemokines, CXC); 0 (Membrane Proteins); 0 (Receptors, Scavenger); 0 (TSPAN17 protein, human); 0 (TSPAN5 protein, human); 0 (Tetraspanins); 0 (cadherin 5); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170611
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600713


  8 / 5219 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28389593
[Au] Autor:Oka T; Sugaya M; Takahashi N; Takahashi T; Shibata S; Miyagaki T; Asano Y; Sato S
[Ad] Endereço:Department of Dermatology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan.
[Ti] Título:CXCL17 Attenuates Imiquimod-Induced Psoriasis-like Skin Inflammation by Recruiting Myeloid-Derived Suppressor Cells and Regulatory T Cells.
[So] Source:J Immunol;198(10):3897-3908, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CXCL17 is expressed in a variety of cancers and promotes tumor progression by recruiting myeloid-derived suppressor cells (MDSCs). MDSCs suppress tumor immunity by attracting regulatory T cells (Tregs) into tumor sites through CCL5. In this study, we examined the role of CXCL17 in skin disorders. CXCL17 mRNA levels in psoriasis skin, but not in lesional skin of atopic dermatitis or cutaneous T cell lymphoma, were significantly higher than those in normal skin. CXCL17 was mainly expressed in the epidermis, and IFN-γ dose-dependently increased CXCL17 expression by human keratinocytes in vitro. As CXCL17 mRNA expression was increased by treatment with imiquimod (IMQ), we examined the effects of CXCL17 in IMQ-induced psoriasis-like skin inflammation. Injection of recombinant CXCL17 into the ear before and during IMQ application decreased ear thickness, inflammatory cytokine expression, and the number of infiltrating cells compared with PBS injection. Flow cytometric analysis and immunofluorescent staining revealed that the numbers of MDSCs, which are CD11b Gr-1 , and that of Tregs, which are CD4 CD25 , were higher in the ear of the CXCL17-injected mice than in PBS-injected mice. MDSCs, but not Tregs, showed chemotaxis to CXCL17 in vitro. When mice were injected with anti-CCL5 Ab or anti-CCL4 Ab simultaneously with recombinant CXCL17, ear thickness and cytokine expression increased to a similar level of mice treated with PBS and control IgG, suggesting that these chemokines were important for anti-inflammatory effects. Taken together, CXCL17 attenuates IMQ-induced psoriasis-like skin inflammation by recruiting MDSCs and Tregs, which may be important for regulating excessive inflammation in psoriasis skin.
[Mh] Termos MeSH primário: Aminoquinolinas/farmacologia
Quimiocinas CXC/imunologia
Quimiocinas/imunologia
Células Supressoras Mieloides/fisiologia
Pele/efeitos dos fármacos
Pele/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CCL4/imunologia
Quimiocina CCL5/imunologia
Quimiocinas/genética
Quimiotaxia
Citocinas/genética
Citocinas/imunologia
Dermatite/tratamento farmacológico
Dermatite/imunologia
Epiderme/efeitos dos fármacos
Epiderme/imunologia
Seres Humanos
Queratinócitos/efeitos dos fármacos
Queratinócitos/imunologia
Camundongos
Células Supressoras Mieloides/efeitos dos fármacos
Células Supressoras Mieloides/imunologia
Psoríase/tratamento farmacológico
Psoríase/imunologia
Pele/patologia
Linfócitos T Reguladores/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (CXCL17 protein, human); 0 (CXCL17 protein, mouse); 0 (Ccl5 protein, mouse); 0 (Chemokine CCL4); 0 (Chemokine CCL5); 0 (Chemokines); 0 (Chemokines, CXC); 0 (Cytokines); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170409
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601607


  9 / 5219 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28382159
[Au] Autor:Lee HT; Liu SP; Lin CH; Lee SW; Hsu CY; Sytwu HK; Hsieh CH; Shyu WC
[Ad] Endereço:Department of Neurosurgery, Taichung Veterans General Hospital, Taichung, Taiwan 40421.
[Ti] Título:A Crucial Role of CXCL14 for Promoting Regulatory T Cells Activation in Stroke.
[So] Source:Theranostics;7(4):855-875, 2017.
[Is] ISSN:1838-7640
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Inflammatory processes have a detrimental role in the pathophysiology of ischemic stroke. However, little is known about the endogenous anti-inflammatory mechanisms in ischemic brain. Here, we identify CXCL14 as a critical mediator of these mechanisms. CXCL14 levels were upregulated in the ischemic brains of humans and rodents. Moreover, hypoxia inducible factor-1α (HIF-1α) drives hypoxia- or cerebral ischemia (CI)-dependent CXCL14 expression via directly binding to the CXCL14 promoter. Depletion of CXCL14 inhibited the accumulation of immature dendritic cells (iDC) or regulatory T cells (Treg) and increased the infarct volume, whereas the supplementation of CXCL14 had the opposite effects. CXCL14 promoted the adhesion, migration, and homing of circulating CD11c iDC to the ischemic tissue via the upregulation of the cellular prion protein (PrP ), PECAM-1, and MMPs. The accumulation of Treg in ischemic areas of the brain was mediated through a cooperative effect of CXCL14 and iDC-secreted IL-2-induced Treg differentiation. Interestingly, CXCL14 largely promoted IL-2-induced Treg differentiation. These findings indicate that CXCL14 is a critical immunomodulator involved in the stroke-induced inflammatory reaction. Passive CXCL14 supplementation provides a tractable path for clinical translation in the improvement of stroke-induced neuroinflammation.
[Mh] Termos MeSH primário: Quimiocinas CXC/metabolismo
Ativação Linfocitária
Acidente Vascular Cerebral/fisiopatologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Células Dendríticas/imunologia
Seres Humanos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL14 protein, human); 0 (Chemokines, CXC)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.7150/thno.17558


  10 / 5219 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28362325
[Au] Autor:Sakumoto R; Hayashi KG; Fujii S; Kanahara H; Hosoe M; Furusawa T; Kizaki K
[Ad] Endereço:Division of Animal Breeding and Reproduction Research, Institute of Livestock and Grassland Science, National Agriculture and Food Research Organization (NARO), Ibaraki 305-0901, Japan. sakumoto@affrc.go.jp.
[Ti] Título:Possible Roles of CC- and CXC-Chemokines in Regulating Bovine Endometrial Function during Early Pregnancy.
[So] Source:Int J Mol Sci;18(4), 2017 Mar 31.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The aim of the present study was to determine the possible roles of chemokines in regulating bovine endometrial function during early pregnancy. The expression of six chemokines, including CCL2, CCL8, CCL11, CCL14, CCL16, and CXCL10, was higher in the endometrium at 15 and 18 days of pregnancy than at the same days in non-pregnant animals. Immunohistochemical staining showed that chemokine receptors (CCR1, CCR2, CCR3, and CXCR3) were expressed in the epithelial cells and glandular epithelial cells of the bovine endometrium as well as in the fetal trophoblast obtained from a cow on day 18 of pregnancy. The addition of interferon-τ (IFNT) to an endometrial tissue culture system increased CCL8 and CXCL10 expression in the tissues, but did not affect CCL2, CCL11, and CCL16 expression. CCL14 expression by these tissues was inhibited by IFNT. CCL16, but not other chemokines, clearly stimulated interferon-stimulated gene 15 (ISG15) and myxovirus-resistance gene 1 (MX1) expression in these tissues. Cyclooxygenase 2 (COX2) expression decreased after stimulation with CCL8 and CCL14, and oxytocin receptor (OTR) expression was decreased by CCL2, CCL8, CCL14, and CXCL10. Collectively, the expression of chemokine genes is increased in the endometrium during early pregnancy. These genes may contribute to the regulation of endometrial function by inhibiting COX2 and OTR expression, subsequently decreasing prostaglandin production and preventing luteolysis in cows.
[Mh] Termos MeSH primário: Quimiocinas CC/genética
Quimiocinas CXC/genética
Endométrio/metabolismo
Células Epiteliais/metabolismo
[Mh] Termos MeSH secundário: Animais
Bovinos
Células Cultivadas
Quimiocinas CC/metabolismo
Quimiocinas CC/fisiologia
Quimiocinas CXC/metabolismo
Quimiocinas CXC/fisiologia
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/metabolismo
Implantação do Embrião/genética
Implantação do Embrião/fisiologia
Endométrio/citologia
Endométrio/fisiologia
Feminino
Perfilação da Expressão Gênica/métodos
Imuno-Histoquímica
Gravidez
Receptores de Quimiocinas/genética
Receptores de Quimiocinas/metabolismo
Receptores de Ocitocina/genética
Receptores de Ocitocina/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Tempo
Técnicas de Cultura de Tecidos
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines, CC); 0 (Chemokines, CXC); 0 (Receptors, Chemokine); 0 (Receptors, Oxytocin); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE



página 1 de 522 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde