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[PMID]:28453765
[Au] Autor:Marafini I; Monteleone I; Dinallo V; Di Fusco D; De Simone V; Laudisi F; Fantini MC; Di Sabatino A; Pallone F; Monteleone G
[Ad] Endereço:Department of Systems Medicine, University of Rome 'Tor Vergata', Rome, Italy.
[Ti] Título:CCL20 Is Negatively Regulated by TGF-ß1 in Intestinal Epithelial Cells and Reduced in Crohn's Disease Patients With a Successful Response to Mongersen, a Smad7 Antisense Oligonucleotide.
[So] Source:J Crohns Colitis;11(5):603-609, 2017 May 01.
[Is] ISSN:1876-4479
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background and Aims: The chemokine CCL20 is over-produced in epithelium of Crohn's disease [CD] patients and contributes to recruiting immune cells to inflamed gut. Tumour necrosis factor-α [TNF-α] is a powerful inducer of CCL20 in intestinal epithelial cells. In CD, high levels of Smad7 block the activity of transforming growth factor-ß1 [TGF-ß1], a negative regulator of TNF signalling. We investigated whether intestinal epithelial cell-derived CCL20 is negatively regulated by TGF-ß1 and whether Smad7 knock-down reduces CCL20 in CD. Methods: CCL20 was evaluated in NCM460, a normal colonic epithelial cell line, stimulated with TGF-ß1 and TNF-α, and in Smad7 over-expressing NCM460 cells. CCL20 and Smad7 expression were assessed in sections of CD intestinal specimens by immunochemistry, and in CD colonic explants treated with mongersen, a Smad7 antisense oligonucleotide. CCL20 was examined in serum samples taken from 95 of 166 active CD patients receiving mongersen or placebo for 2 weeks and participating in a phase II, multicentre, double-blind, placebo-controlled study. Results: CCL20 expression was increased by TNF-α, and this effect was inhibited by TGF-ß1 in NCM460 cells, but not in Smad7 over-expressing NCM460 cells. In CD, epithelium CCL20 and Smad7 co-localised, and treatment of CD explants with mongersen reduced CCL20 production. During follow-up, in responders to mongersen, serum CCL20 levels significantly decreased, whereas patients without response/remission to mongersen and placebo patients did not have change in CCL20. Conclusions: TGF-ß1 reduces intestinal epithelial cell-derived CCL20 production, an effect abrogated by Smad7. CD patients responding to mongersen demonstrated a reduction in serum CCL20.
[Mh] Termos MeSH primário: Quimiocina CCL20/metabolismo
Doença de Crohn/tratamento farmacológico
Mucosa Intestinal/metabolismo
Oligonucleotídeos/uso terapêutico
Proteína Smad7/antagonistas & inibidores
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Quimiocina CCL20/sangue
Doença de Crohn/metabolismo
Método Duplo-Cego
Seres Humanos
Mucosa Intestinal/efeitos dos fármacos
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (CCL20 protein, human); 0 (Chemokine CCL20); 0 (GED0301); 0 (Oligonucleotides); 0 (SMAD7 protein, human); 0 (Smad7 Protein); 0 (Transforming Growth Factor beta1)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1093/ecco-jcc/jjw191


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[PMID]:28746740
[Au] Autor:McDonald KG; Wheeler LW; McDole JR; Joerger S; Gustafsson JK; Kulkarni DH; Knoop KA; Williams IR; Miller MJ; Newberry RD
[Ad] Endereço:Department of Internal Medicine, Washington University School of Medicine, St Louis, MO, USA.
[Ti] Título:CCR6 promotes steady-state mononuclear phagocyte association with the intestinal epithelium, imprinting and immune surveillance.
[So] Source:Immunology;152(4):613-627, 2017 12.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The intestinal lamina propria (LP) contains antigen-presenting cells with features of dendritic cells and macrophages, collectively referred to as mononuclear phagocytes (MNPs). Association of MNPs with the epithelium is thought to play an important role in multiple facets of intestinal immunity including imprinting MNPs with the ability to induce IgA production, inducing the expression of gut homing molecules on T cells, facilitating the capture of luminal antigens and microbes, and subsequent immune responses in the mesenteric lymph node (MLN). However, the factors promoting this process in the steady state are largely unknown, and in vivo models to test and confirm the importance of LP-MNP association with the epithelium for these outcomes are unexplored. Evaluation of epithelial expression of chemoattractants in mice where MNP-epithelial associations were impaired suggested CCL20 as a candidate promoting epithelial association. Expression of CCR6, the only known receptor for CCL20, was required for MNPs to associate with the epithelium. LP-MNPs from CCR6 mice did not display defects in acquiring antigen and stimulating T-cell responses in ex vivo assays or in responses to antigen administered systemically. However, LP-MNPs from CCR6-deficient mice were impaired at acquiring luminal and epithelial antigens, inducing IgA production in B cells, inducing immune responses in the MLN, and capturing and trafficking luminal commensal bacteria to the MLN. These findings identify a crucial role for CCR6 in promoting LP-MNPs to associate with the intestinal epithelium in the steady state to perform multiple functions promoting gut immune homeostasis.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Impressão Genômica/imunologia
Vigilância Imunológica
Mucosa Intestinal/imunologia
Macrófagos/imunologia
Receptores CCR6/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/citologia
Linfócitos B/imunologia
Quimiocina CCL20/genética
Quimiocina CCL20/imunologia
Células Dendríticas/citologia
Seres Humanos
Macrófagos/citologia
Camundongos
Camundongos Knockout
Receptores CCR6/genética
Linfócitos T/citologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CCL20 protein, mouse); 0 (CCR6 protein, mouse); 0 (Chemokine CCL20); 0 (Receptors, CCR6)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12801


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[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


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[PMID]:28708859
[Au] Autor:Couderc E; Morel F; Levillain P; Buffière-Morgado A; Camus M; Paquier C; Bodet C; Jégou JF; Pohin M; Favot L; Garcia M; Huguier V; Mcheik J; Lacombe C; Yssel H; Guillet G; Bernard FX; Lecron JC
[Ad] Endereço:Laboratoire Inflammation, Tissus Epithéliaux et Cytokines, UPRES EA4331, Pôle Biologie Santé, Université de Poitiers, TSA, POITIERS, France.
[Ti] Título:Interleukin-17A-induced production of acute serum amyloid A by keratinocytes contributes to psoriasis pathogenesis.
[So] Source:PLoS One;12(7):e0181486, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute-serum Amyloid A (A-SAA), one of the major acute-phase proteins, is mainly produced in the liver but extra-hepatic synthesis involving the skin has been reported. Its expression is regulated by the transcription factors NF-κB, C/EBPß, STAT3 activated by proinflammatory cytokines. OBJECTIVES: We investigated A-SAA synthesis by resting and cytokine-activated Normal Human Epidermal Keratinocytes (NHEK), and their inflammatory response to A-SAA stimulation. A-SAA expression was also studied in mouse skin and liver in a model mimicking psoriasis and in the skin and sera of psoriatic and atopic dermatitis (AD) patients. METHODS: NHEK were stimulated by A-SAA or the cytokines IL-1α, IL-17A, IL-22, OSM, TNF-α alone or in combination, previously reported to reproduce features of psoriasis. Murine skins were treated by imiquimod cream. Human skins and sera were obtained from patients with psoriasis and AD. A-SAA mRNA was quantified by RT qPCR. A-SAA proteins were dosed by ELISA or immunonephelemetry assay. RESULTS: IL-1α, TNF-α and mainly IL-17A induced A-SAA expression by NHEK. A-SAA induced its own production and the synthesis of hBD2 and CCL20, both ligands for CCR6, a chemokine receptor involved in the trafficking of Th17 lymphocytes. A-SAA expression was increased in skins and livers from imiquimod-treated mice and in patient skins with psoriasis, but not significantly in those with AD. Correlations between A-SAA and psoriasis severity and duration were observed. CONCLUSION: Keratinocytes could contribute to psoriasis pathogenesis via A-SAA production, maintaining a cutaneous inflammatory environment, activating innate immunity and Th17 lymphocyte recruitment.
[Mh] Termos MeSH primário: Dermatite Atópica/patologia
Interleucina-17/farmacologia
Psoríase/patologia
Proteína Amiloide A Sérica/metabolismo
Pele/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Idoso
Aminoquinolinas/farmacologia
Animais
Células Cultivadas
Quimiocina CCL20/metabolismo
Quimiocina CCL20/farmacologia
Citocinas/genética
Citocinas/metabolismo
Dermatite Atópica/metabolismo
Modelos Animais de Doenças
Feminino
Seres Humanos
Interleucina-17/genética
Interleucina-17/metabolismo
Queratinócitos/citologia
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Psoríase/metabolismo
Receptores CCR6/metabolismo
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/isolamento & purificação
Proteínas Recombinantes/farmacologia
Proteína Amiloide A Sérica/análise
Proteína Amiloide A Sérica/genética
Pele/metabolismo
Células Th17/citologia
Células Th17/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (Chemokine CCL20); 0 (Cytokines); 0 (Interleukin-17); 0 (Receptors, CCR6); 0 (Recombinant Proteins); 0 (Serum Amyloid A Protein); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181486


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[PMID]:28651743
[Au] Autor:Ye JF; Qi WX; Liu MY; Li Y
[Ad] Endereço:Key Laboratory of Zoonoses Research, Ministry of Education, Institute of Zoonosis, Department of Hepato-Biliary-Pancreatic Surgery, First Hospital, Jilin University, Changchun 130062, PR China.
[Ti] Título:The combination of NK and CD8+T cells with CCL20/IL15-armed oncolytic adenoviruses enhances the growth suppression of TERT-positive tumor cells.
[So] Source:Cell Immunol;318:35-41, 2017 Aug.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Adoptive immunotherapy and targeted gene therapy have been extensively used to eliminate tumor cells. The combination treatment is capable of efficiently generating an effective antitumor immune response and disrupting tumor-induced tolerance. Moreover, effective antitumor immune responses are dependent on coordinate interaction among various effector cells. This study focused on whether the combination of cytotoxic effector cell-based adoptive immunotherapy and CCL20/IL15-armed oncolytic adenoviruses could induce enhanced antitumor activity. The CCL20/IL15-armed oncolytic adenovirus was constructed using homologous recombination with shuttle plasmids and full-length Ad backbones. We chose the telomerase reverse transcriptase promoter (TERTp) to replace the E1A promoter to drive the oncolytic adenoviral E1A gene. Thus, this CRAd-CCL20-IL15 could induce apoptosis in TERTp-positive tumor cells due to viral propagation, but these viruses could not replicate efficiently in normal cells. The combination of cytotoxic effector cells and CRAd-CCL20-IL15 showed greater antitumor potential than that of cytotoxic effector cells or CRAd-CCL20-IL15 alone. Moreover, the combined treatment could induce tumor-specific cytotoxicity of CTLs in vitro. Further analysis demonstrated that this combined treatment resulted in significant tumor regression in mouse models. This study has provided preclinical evidence that combined treatment with cytotoxic effector cells and CRAd-CCL20-IL15 may offer alternative treatment options for tumor therapy.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Vacinas Anticâncer/imunologia
Imunoterapia/métodos
Células Matadoras Naturais/imunologia
Neoplasias/terapia
[Mh] Termos MeSH secundário: Adenoviridae/genética
Animais
Linfócitos T CD8-Positivos/transplante
Processos de Crescimento Celular
Linhagem Celular Tumoral
Quimiocina CCL20/genética
Quimiocina CCL20/metabolismo
Terapia Combinada
Vetores Genéticos/genética
Seres Humanos
Imunidade
Interleucina-15/genética
Interleucina-15/metabolismo
Células Matadoras Naturais/transplante
Camundongos
Camundongos SCID
Transplante de Neoplasias
Neoplasias/imunologia
Telomerase/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cancer Vaccines); 0 (Chemokine CCL20); 0 (Interleukin-15); EC 2.7.7.49 (TERT protein, human); EC 2.7.7.49 (Telomerase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE


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[PMID]:28628664
[Au] Autor:Alvarez-Simón D; Muñoz X; Gómez-Ollés S; de Homdedeu M; Untoria MD; Cruz MJ
[Ad] Endereço:Pulmonology Service, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
[Ti] Título:Effects of diesel exhaust particle exposure on a murine model of asthma due to soybean.
[So] Source:PLoS One;12(6):e0179569, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Exposure to soybean allergens has been linked to asthma outbreaks. Exposure to diesel exhaust particles (DEP) has been associated with an increase in the risk of asthma and asthma exacerbation; however, in both cases the underlying mechanisms remain poorly understood, as does the possible interaction between the two entities. OBJECTIVE: To investigate how the combination of soybean allergens and DEP can affect the induction or exacerbation of asthma in a murine model. METHODS: BALB/c mice received intranasal instillations of saline, 3 or 5 mg protein/ml soybean hull extract (SHE), or a combination of one of these three solutions with DEP. Airway hyperresponsiveness (AHR), pulmonary inflammation in bronchoalveolar lavage, total serum immunoglobulin E and histological studies were assessed. RESULTS: A 5 mg protein/ml SHE solution was able by itself to enhance AHR (p = 0.0033), increase eosinophilic inflammation (p = 0.0003), increase levels of IL-4, IL-5, IL-13, IL-17A, IL-17F and CCL20, and reduce levels of IFN-γ. The combination of 5 mg protein/ml SHE with DEP also produced an increase in AHR and eosinophilic inflammation, but presented a slightly different cytokine profile with higher levels of Th17-related cytokines. However, while the 3 mg protein/ml SHE solution did not induce asthma, co-exposure with DEP resulted in a markedly enhanced AHR (p = 0.002) and eosinophilic inflammation (p = 0.004), with increased levels of IL-5, IL-17F and CCL20 and decreased levels of IFN-γ. CONCLUSIONS & CLINICAL RELEVANCE: The combination of soybean allergens and DEP is capable of triggering an asthmatic response through a Th17-related mechanism when the soybean allergen concentration is too low to promote a response by itself. DEP monitoring may be a useful addition to allergen monitoring in order to prevent new asthma outbreaks.
[Mh] Termos MeSH primário: Alérgenos/toxicidade
Asma/etiologia
Material Particulado/toxicidade
Feijão de Soja/metabolismo
Emissões de Veículos/toxicidade
[Mh] Termos MeSH secundário: Administração por Inalação
Animais
Área Sob a Curva
Asma/patologia
Líquido da Lavagem Broncoalveolar/química
Líquido da Lavagem Broncoalveolar/citologia
Quimiocina CCL20/sangue
Citocinas/sangue
Modelos Animais de Doenças
Eosinófilos/citologia
Eosinófilos/imunologia
Eosinófilos/metabolismo
Feminino
Imunoglobulina E/sangue
Pulmão/fisiologia
Camundongos
Camundongos Endogâmicos BALB C
Curva ROC
Hipersensibilidade Respiratória/etiologia
Hipersensibilidade Respiratória/patologia
Células Th17/imunologia
Células Th17/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Chemokine CCL20); 0 (Cytokines); 0 (Particulate Matter); 0 (Vehicle Emissions); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179569


  7 / 721 MEDLINE  
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[PMID]:28619514
[Au] Autor:Thu Le HP; Nakamura Y; Oh-Oka K; Ishimaru K; Nakajima S; Nakao A
[Ad] Endereço:Department of Immunology, University of Yamanashi Faculty of Medicine, 1110 Shimokato, Chuo, Yamanashi 409-3898, Japan.
[Ti] Título:The frequency of Th17 cells in the small intestine exhibits a day-night variation dependent on circadian clock activity.
[So] Source:Biochem Biophys Res Commun;490(2):290-295, 2017 Aug 19.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin-17-producing CD4 T helper (Th17) cells are a key immune lineage that protects against bacterial and fungal infections at mucosal surfaces. At steady state, Th17 cells are abundant in the small intestinal mucosa of mice. There are several mechanisms for regulating the population of Th17 cells in the small intestine, reflecting the importance of maintaining their numbers in the correct balance. Here we demonstrate the existence of a time-of-day-dependent variation in the frequency of Th17 cells in the lamina propria of the small intestine in wild-type mice, which was not observed in mice with a loss-of-function mutation of the core circadian gene Clock or in mice housed under aberrant light/dark conditions. Consistent with this, expression of CCL20, a chemokine that regulates homeostatic trafficking of Th17 cells to the small intestine, exhibited circadian rhythms in the small intestine of wild-type, but not Clock-mutated, mice. In support of these observations, the magnitude of ovalbumin (OVA)-specific antibody and T-cell responses in mice sensitized with OVA plus cholera toxin, a mucosal Th17 cell-dependent adjuvant, was correlated with daily variations in the proportion of Th17 cells in the small intestine. These results suggest that the proportion of Th17 cells in the small intestine exhibits a day-night variation in association with CCL20 expression, which depends on circadian clock activity. The findings provide novel insight into the regulation of the Th17 cell population in the small intestine at steady state, which may have translational potential for mucosal vaccination strategies.
[Mh] Termos MeSH primário: Relógios Circadianos/fisiologia
Intestino Delgado/citologia
Células Th17/citologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CCL20/genética
Quimiocina CCL20/metabolismo
Relógios Circadianos/imunologia
Feminino
Intestino Delgado/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Células Th17/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL20 protein, mouse); 0 (Chemokine CCL20)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE


  8 / 721 MEDLINE  
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[PMID]:28618084
[Au] Autor:Muscella A; Vetrugno C; Marsigliante S
[Ad] Endereço:Dipartimento di Scienze e Tecnologie Biologiche e Ambientali (Di.S.Te.B.A.), Università del Salento, Lecce, Italy.
[Ti] Título:CCL20 promotes migration and invasiveness of human cancerous breast epithelial cells in primary culture.
[So] Source:Mol Carcinog;56(11):2461-2473, 2017 Nov.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The relation between the tumor and its microenvironment is one of the most interesting and less understood issues. Recently, we showed a role of CCL20 chemokine in proning the healthy tissue neighboring the tumor to carcinogenesis. Besides, tumor-secreted CCL20 induced proliferation, migration, and EMT of healthy cells. In this context, we have studied here if CCL20 had effects on the migration of cancer cells and the intracellular pathways used in breast epithelial cells in primary culture. Using molecular (siRNA) and pharmacological (inhibitors) techniques, we found multiple signaling kinases to be activated and involved in CCL20-induced tumor breast cell migration. CCL20 provoked a 2.5-fold increase of cell migration and invasion; CCL20 also enhanced MMP- 2 and MMP-9 mRNAs/protein expression and activities. Cell migration and invasiveness due to CCL20 significantly decreased when MMP-2 and MMP-9 were inhibited in CCL20-stimulated cells. CCL20 controlled MMP-2 expression through the JAK2/STAT3 pathway, while the expression of MMP-9 occurred by PKC-α that activated, consequently, c-Src, Akt, and finally NF-kB. These results reveal a role for CCL20 also in tumor breast cell and point to CCL20 as a novel therapeutic target in cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Mama/patologia
Movimento Celular
Quimiocina CCL20/genética
Células Epiteliais/patologia
Regulação Neoplásica da Expressão Gênica
[Mh] Termos MeSH secundário: Mama/metabolismo
Neoplasias da Mama/genética
Neoplasias da Mama/imunologia
Linhagem Celular Tumoral
Quimiocina CCL20/imunologia
Células Epiteliais/imunologia
Células Epiteliais/metabolismo
Feminino
Seres Humanos
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/imunologia
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/imunologia
NF-kappa B/imunologia
Invasividade Neoplásica/genética
Invasividade Neoplásica/patologia
Proteínas Proto-Oncogênicas c-akt/imunologia
Transdução de Sinais
Células Tumorais Cultivadas
Quinases da Família src/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL20 protein, human); 0 (Chemokine CCL20); 0 (NF-kappa B); EC 2.7.10.2 (CSK tyrosine-protein kinase); EC 2.7.10.2 (src-Family Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22693


  9 / 721 MEDLINE  
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[PMID]:28600287
[Au] Autor:Lee JJ; Kao KC; Chiu YL; Jung CJ; Liu CJ; Cheng SJ; Chang YL; Ko JY; Chia JS
[Ad] Endereço:Department of Oral Maxillofacial Surgery, National Taiwan University Hospital, Taipei 100, Taiwan.
[Ti] Título:Enrichment of Human CCR6 Regulatory T Cells with Superior Suppressive Activity in Oral Cancer.
[So] Source:J Immunol;199(2):467-476, 2017 Jul 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human oral squamous cell carcinoma (OSCC) constitutes an inflammatory microenvironment enriched with chemokines such as CCL20, which promote cancer cell invasion and tumor progression. We found that in OSCC there is a correlation between the expression of and mRNA. Therefore, we hypothesized that OSCC may favor the recruitment and retention of regulatory T (Treg) cells that express the CCL20 receptor, CCR6. Interestingly, most (∼60%) peripheral blood Treg cells express CCR6, and CCR6 Treg cells exhibit an activated effector/memory phenotype. In contrast, a significant portion (>30%) of CCR6 Treg cells were found to be CD45RA naive Treg cells. Compared to CCR6 naive or memory Treg cells, CCR6 Treg cells exhibit stronger suppressive activity and display higher FOXP3 expression along with lower methylation at the Treg-specific demethylated region of the gene. This predominance of CCR6 Treg cells was also found in the draining lymph nodes and tumor-infiltrating lymphocytes of OSCC patients with early or late clinical staging. Moreover, CCR6 Treg cells isolated from tumor-infiltrating lymphocytes or draining lymph nodes maintained similar phenotypic and suppressive characteristics ex vivo as did their counterparts isolated from peripheral blood. These results suggest that CCR6 marks activated effector or memory Treg phenotypes with superior suppressive activity in humans.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/imunologia
Neoplasias Bucais/imunologia
Receptores CCR6/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Adulto
Carcinoma de Células Escamosas/patologia
Quimiocina CCL20/genética
Quimiocina CCL20/imunologia
Feminino
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/imunologia
Seres Humanos
Memória Imunológica
Antígenos Comuns de Leucócito/genética
Antígenos Comuns de Leucócito/imunologia
Linfonodos/citologia
Linfonodos/imunologia
Linfócitos do Interstício Tumoral/imunologia
Masculino
Metilação
Meia-Idade
Receptores CCR6/deficiência
Receptores CCR6/genética
Linfócitos T Reguladores/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL20 protein, human); 0 (Chemokine CCL20); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (Receptors, CCR6); EC 3.1.3.48 (Leukocyte Common Antigens)
[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.1601815


  10 / 721 MEDLINE  
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[PMID]:28599122
[Au] Autor:Shi T; He Y; Sun W; Wu Y; Li L; Jie Z; Su X
[Ad] Endereço:Department of Respiratory Medicine, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, 200240, China.
[Ti] Título:Respiratory Syncytial virus infection compromises asthma tolerance by recruiting interleukin-17A-producing cells via CCR6-CCL20 signaling.
[So] Source:Mol Immunol;88:45-57, 2017 Aug.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Asthma tolerance can be induced by breast-feeding or oral feeding with ovalbumin (OVA). Anergy or deletion of specific T cells and generation of T regulatory cells might contribute to this process. However, whether respiratory syncytial virus (RSV) infection would affect asthma tolerance is not very clear. Here, we first established asthma and oral tolerance mouse models and then analyzed airway hypersensitivity and asthma-related genes in the lung, CCR6-expressing IL-17A cells in the lungs, hilar or mesenteric lymph nodes (HLN or MLN) among control, asthmatic, tolerized, RSV infection, and RSV-infected asthmatic and tolerized groups. We also administrated CCL20 or IL-17A neutralizing antibody to RSV-infected tolerized mice to test whether RSV infection would mobilize CCR6-expressing IL-17A cells from MLN to the infected lungs. We found that tolerized mice infected with RSV developed asthma-like responses manifested by increasing airway hypersensitivity, exacerbating peribronchial inflammation, elevating lung asthma-related genes (Il17a, Mu5ac, and Gob5), accumulating CCR6-expressing IL-17A cells in the lungs and HLN with a reduction of this cell population in MLN. CCL20-CCR6 co-expression in RSV-infected tolerized MLN was reduced. Neutralization of CCL20 reduced CD3 CD4 CCR6 cells in the RSV-infected tolerized HLN. Neutralization of IL-17A mitigated the compromising effects of RSV infection on asthma tolerance. Taken together, RSV infection impairs asthma tolerance by recruiting IL-17A-producing cells via CCR6-CCL20 signaling. The findings provide novel insight into exacerbation and therapeutic strategy of asthma under RSV infection.
[Mh] Termos MeSH primário: Asma/imunologia
Quimiocina CCL20/imunologia
Tolerância Imunológica/imunologia
Interleucina-17/imunologia
Receptores CCR6/imunologia
Infecções por Vírus Respiratório Sincicial/imunologia
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar/imunologia
Complexo CD3/metabolismo
Antígenos CD4/metabolismo
Linhagem Celular Tumoral
Canais de Cloreto/genética
Feminino
Imunoglobulina E/sangue
Interleucina-17/genética
Pulmão/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Mucoproteínas/genética
Ovalbumina/imunologia
Infecções por Vírus Respiratório Sincicial/virologia
Vírus Sinciciais Respiratórios/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL20 protein, mouse); 0 (CCR6 protein, mouse); 0 (CD3 Complex); 0 (CD4 Antigens); 0 (Chemokine CCL20); 0 (Chloride Channels); 0 (Clca3 protein, mouse); 0 (Il17a protein, mouse); 0 (Interleukin-17); 0 (Mucoproteins); 0 (Receptors, CCR6); 37341-29-0 (Immunoglobulin E); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE



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