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[PMID]:28668835
[Au] Autor:Furudate S; Fujimura T; Kambayashi Y; Kakizaki A; Hidaka T; Aiba S
[Ad] Endereço:Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Japan.
[Ti] Título:Immunomodulatory Effect of Imiquimod Through CCL22 Produced by Tumor-associated Macrophages in B16F10 Melanomas.
[So] Source:Anticancer Res;37(7):3461-3471, 2017 07.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Tumor-associated macrophages (TAMs), together with splenic CD11b cells, help maintain the tumor microenvironment. The immunomodulatory compound imiquimod (IQM) stimulates innate immune cells, including macrophages, to induce antitumor effects. In order to elucidate the effects of IQM on the tumor microenvironment, we investigated the immunomodulatory effect of IQM during melanoma growth by using the B16F10 melanoma model. MATERIALS AND METHODS: To elucidate the immunomodulatory effects of IQM on the tumor microenvironment, we isolated CD11b TAMs and splenic CD11b cells and evaluated the immunomodulatory effects of IQM, using the B16F10 melanoma model. RESULTS: IQM suppressed B16F10 melanoma growth in parallel with reduction of Foxp3 regulatory T cells (Tregs) at the tumor site, caused by the down-regulation of CCL22 production by tumor-derived and splenic CD11b cells. Subsequently, we investigated the antitumor or tumor-loading effects of splenic CD11b cells on B16F10 melanoma growth in vivo. B16F10 melanoma growth was accelerated by splenic CD11b cells from untreated mice, but was inhibited by splenic CD11b cells from IQM-treated mice. Consistent with these results, Foxp3 Tregs were significantly decreased in tumors of mice implanted with both melanoma and splenic CD11b cells from topical IQM-treated mice. Furthermore, intratumoral administration of anti-CCL22 antibody inhibited B16F10 melanoma growth by decreasing Treg recruitment at the tumor site. CONCLUSION: Our results suggest a possible mechanism for the antitumor immune response induced by IQM through tumor-associated macrophages.
[Mh] Termos MeSH primário: Aminoquinolinas/imunologia
Aminoquinolinas/farmacologia
Quimiocina CCL22/metabolismo
Fatores Imunológicos/imunologia
Macrófagos/efeitos dos fármacos
Melanoma Experimental/dietoterapia
Melanoma Experimental/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígeno CD11b/imunologia
Antígeno CD11b/metabolismo
Linhagem Celular Tumoral
Quimiocina CCL22/imunologia
Regulação para Baixo/efeitos dos fármacos
Regulação para Baixo/imunologia
Feminino
Fatores de Transcrição Forkhead/imunologia
Fatores de Transcrição Forkhead/metabolismo
Fatores Imunológicos/farmacologia
Macrófagos/imunologia
Melanoma Experimental/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Carga Tumoral/efeitos dos fármacos
Carga Tumoral/imunologia
Microambiente Tumoral/efeitos dos fármacos
Microambiente Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (CD11b Antigen); 0 (Ccl22 protein, mouse); 0 (Chemokine CCL22); 0 (Forkhead Transcription Factors); 0 (Immunologic Factors); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170703
[St] Status:MEDLINE


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[PMID]:28501127
[Au] Autor:Wei Y; Wang T; Song H; Tian L; Lyu G; Zhao L; Xue Y
[Ad] Endereço:Department of Gastrointestinal Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang Province, China.
[Ti] Título:C-C motif chemokine 22 ligand (CCL22) concentrations in sera of gastric cancer patients are related to peritoneal metastasis and predict recurrence within one year after radical gastrectomy.
[So] Source:J Surg Res;211:266-278, 2017 May 01.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Gastric cancer is a common cancer with a poor prognosis. Chemokines play important roles in the tumor microenvironments to support tumor growth and metastasis. The effects of C-C motif chemokine ligand 22 (CCL22) in gastric cancer remain unclear. MATERIALS AND METHODS: Between January 1, 2014 and April 31, 2014, a total of 298 gastric cancer patients were recruited to this study. Circulating concentrations of CCL22 were measured in gastric cancer patients before surgery, at discharged and during follow-up visits. The expression of CCL22 in gastric cancer tumor beds was measured by immunohistochemistry. The proportion of CD3 CD4 CD25 Foxp3 regulatory T cells in tumor sites was assessed by flow cytometry. RESULTS: Gastric cancer patients had higher serum CCL22 levels compared to healthy controls (P < 0.001). Immunohistochemistry indicated that the gastric cancer tumor beds were the source of serum CCL22, as gastric cancer patients had an increased proportion of strong expression of CCL22 (P < 0.01), and immunohistochemistry scores were positively correlated with levels of circulating CCL22 (P < 0.001). Gastric cancer tissue harbored a higher percentage of regulatory T cells compared to normal tumor-free stomach margins (P < 0.001), and this abundance of regulatory T cells was positively correlated with circulating levels of CCL22 (P < 0.001). Gastric cancer patients with peritoneal metastasis showed increased levels of circulating CCL22 before surgery compared to metastasis-free patients (P < 0.001). Gastric cancer patients with the recurrence within the first year after surgery had elevated serum CCL22 concentrations at different time points compared to those of recurrence-free patients (P < 0.001). Logistic regression analysis indicated that high CCL22 circulating levels before surgery is a risk factor for peritoneal metastasis and an independent risk factor for an early recurrence after surgery. CONCLUSIONS: CCL22 plays an important role in supporting gastric cancer development presumably by increasing the percentage of regulatory T cells in the tumor microenvironments. CCL22 levels in sera have a predictive value for gastric cancer peritoneal metastasis and the early recurrence. Therefore, CCL22 may be a therapeutic target for gastric cancer.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/sangue
Quimiocina CCL22/sangue
Gastrectomia
Recidiva Local de Neoplasia/diagnóstico
Neoplasias Peritoneais/secundário
Neoplasias Gástricas/patologia
Neoplasias Gástricas/cirurgia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Estudos de Casos e Controles
Ensaio de Imunoadsorção Enzimática
Feminino
Seguimentos
Seres Humanos
Imuno-Histoquímica
Modelos Logísticos
Masculino
Meia-Idade
Recidiva Local de Neoplasia/sangue
Neoplasias Peritoneais/sangue
Neoplasias Peritoneais/diagnóstico
Neoplasias Gástricas/sangue
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CCL22 protein, human); 0 (Chemokine CCL22)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170515
[St] Status:MEDLINE


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[PMID]:28324102
[Au] Autor:Pellegrini S; Sordi V; Bolla AM; Saita D; Ferrarese R; Canducci F; Clementi M; Invernizzi F; Mariani A; Bonfanti R; Barera G; Testoni PA; Doglioni C; Bosi E; Piemonti L
[Ad] Endereço:Diabetes Research Institute, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy.
[Ti] Título:Duodenal Mucosa of Patients With Type 1 Diabetes Shows Distinctive Inflammatory Profile and Microbiota.
[So] Source:J Clin Endocrinol Metab;102(5):1468-1477, 2017 May 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Increasing evidences suggest a correlation between gut and type 1 diabetes (T1D). Objective: The objective of this study is to evaluate the gut inflammatory profile and microbiota in patients with T1D compared with healthy control (CTRL) subjects and patients with celiac disease (CD) as gut inflammatory disease controls. Design/Setting/Participants: The inflammatory status and microbiome composition were evaluated in biopsies of the duodenal mucosa of patients with T1D (n = 19), in patients with CD (n = 19), and CTRL subjects (n = 16) recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. Main Outcome Measures: Inflammation was evaluated by gene expression study and immunohistochemistry. Microbiome composition was analyzed by 16S ribosomal RNA gene sequencing. Results: An increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFα, and VEGFA was observed in patients with T1D compared with CTRL subjects and patients with CD. Immunohistochemical analysis confirmed T1D-specific inflammatory status compared with healthy and CD control tissues, mainly characterized by the increase of the monocyte/macrophage lineage infiltration. The T1D duodenal mucosal microbiome results were different from the other groups, with an increase in Firmicutes and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes. The expression of genes specific for T1D inflammation was associated with the abundance of specific bacteria in the duodenum. Conclusions: This study shows that duodenal mucosa in T1D presents disease-specific abnormalities in the inflammatory profile and microbiota. Understanding the mechanisms underlying these features is critical to disentangle the complex pathogenesis of T1D and to gain new perspectives for future therapies targeting the intestine.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/imunologia
Duodeno/imunologia
Microbioma Gastrointestinal/genética
Mucosa Intestinal/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Antígenos CD/genética
Antígenos CD/imunologia
Antígenos de Diferenciação Mielomonocítica/genética
Antígenos de Diferenciação Mielomonocítica/imunologia
Proteína C-Reativa/genética
Proteína C-Reativa/imunologia
Estudos de Casos e Controles
Doença Celíaca/imunologia
Doença Celíaca/microbiologia
Quimiocina CCL19/genética
Quimiocina CCL19/imunologia
Quimiocina CCL22/genética
Quimiocina CCL22/imunologia
Criança
Pré-Escolar
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/imunologia
Diabetes Mellitus Tipo 1/genética
Diabetes Mellitus Tipo 1/microbiologia
Duodeno/microbiologia
Feminino
Seres Humanos
Lactente
Subunidade alfa de Receptor de Interleucina-4/genética
Subunidade alfa de Receptor de Interleucina-4/imunologia
Mucosa Intestinal/microbiologia
Masculino
Meia-Idade
Proteínas Quimioatraentes de Monócitos/genética
Proteínas Quimioatraentes de Monócitos/imunologia
RNA Ribossômico 16S/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptores CCR2/genética
Receptores CCR2/imunologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Componente Amiloide P Sérico/genética
Componente Amiloide P Sérico/imunologia
Transcriptoma
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CCL13 protein, human); 0 (CCL19 protein, human); 0 (CCL22 protein, human); 0 (CCR2 protein, human); 0 (CD68 antigen, human); 0 (Chemokine CCL19); 0 (Chemokine CCL22); 0 (IL4R protein, human); 0 (Interleukin-4 Receptor alpha Subunit); 0 (Monocyte Chemoattractant Proteins); 0 (RNA, Ribosomal, 16S); 0 (Receptors, CCR2); 0 (Serum Amyloid P-Component); 0 (TNF protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 148591-49-5 (PTX3 protein); 9007-41-4 (C-Reactive Protein); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-3222


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[PMID]:28274317
[Au] Autor:Luo Q; Jin Z; Chen S; Yang L; Li B; Li W; Li Y; Wu X
[Ad] Endereço:Institute of Hematology, Medical College, Jinan University, Guangzhou 510632, China.
[Ti] Título:[Changes of TRGV genes and prognosis-related chemokine/receptor gene expressions in T cell lymphoma].
[So] Source:Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi;33(3):362-366, 2017 Mar.
[Is] ISSN:1007-8738
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Objective To analyze the expressions of T cell receptor γ subfamily variable region I, II, and III genes (TRGV I~III) and prognosis-related chemokines and their receptor genes (CCL20, CCR6, CCL17, CCL22 and CCR4) in the peripheral blood of T-cell lymphoma (non-γδ T cell type) patients, and to investigate the correlations between γδ T cells and chemokines/receptors and their relevance to disease prognosis. Methods Peripheral blood samples were collected from 27 patients with T-cell lymphoma (non-γδ T cell type) and 9 healthy individuals as controls. Expressions of TRGV I~III subfamily genes and prognosis-related chemokines/receptors (CCL20/CCR6 and CCL17/CCL22/CCR4) in the peripheral blood of patients with T-cell lymphoma and normal controls were detected by quantitative real-time PCR. Results Compared with the normal controls, the expression levels of TRGV I-III subfamily genes of patients at the stages of initial onset, relapse/refractoriness and complete remission (CR) were significantly higher, and the expression patterns of TRGV subfamilies were changed. The expression levels of CCL22 and CCR4 in initial onset group and relapse/refractory group were significantly higher than that in normal controls, while CCL17 expression was significantly lower than that in normal controls. There were unique correlation patterns in the expressions of TRGV subfamily genes and chemokine/receptor genes in the patients at the stages of initial onset, CR and relapse/refractoriness. There are low expressions of TRGV II subfamilies in newly diagnosed and relapse/refractory T-cell lymphoma patients, and their expressions are elevated after treatment. Conclusion TRGV II subfamilies might be the T cell functional subset against T-cell lymphoma, and might be associated with the outcome of the disease. And the high expression of CCL22/CCR4 might be related to the pathogenesis of T-cell lymphoma.
[Mh] Termos MeSH primário: Quimiocinas/genética
Linfoma de Células T/genética
Receptores de Antígenos de Linfócitos T gama-delta/genética
Receptores de Quimiocinas/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Quimiocina CCL17/genética
Quimiocina CCL17/metabolismo
Quimiocina CCL20/genética
Quimiocina CCL20/metabolismo
Quimiocina CCL22/genética
Quimiocina CCL22/metabolismo
Quimiocinas/metabolismo
Criança
Feminino
Seres Humanos
Linfoma de Células T/metabolismo
Masculino
Meia-Idade
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Receptores CCR4/genética
Receptores CCR4/metabolismo
Receptores CCR6/genética
Receptores CCR6/metabolismo
Receptores de Quimiocinas/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL17 protein, human); 0 (CCL20 protein, human); 0 (CCL22 protein, human); 0 (CCR4 protein, human); 0 (CCR6 protein, human); 0 (Chemokine CCL17); 0 (Chemokine CCL20); 0 (Chemokine CCL22); 0 (Chemokines); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, CCR4); 0 (Receptors, CCR6); 0 (Receptors, Chemokine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE


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[PMID]:28241741
[Au] Autor:Chiu YC; Wang LJ; Lu TP; Hsiao TH; Chuang EY; Chen Y
[Ad] Endereço:Greehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.
[Ti] Título:Differential correlation analysis of glioblastoma reveals immune ceRNA interactions predictive of patient survival.
[So] Source:BMC Bioinformatics;18(1):132, 2017 Feb 28.
[Is] ISSN:1471-2105
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recent studies illuminated a novel role of microRNA (miRNA) in the competing endogenous RNA (ceRNA) interaction: two genes (ceRNAs) can achieve coexpression by competing for a pool of common targeting miRNAs. Individual biological investigations implied ceRNA interaction performs crucial oncogenic/tumor suppressive functions in glioblastoma multiforme (GBM). Yet, a systematic analysis has not been conducted to explore the functional landscape and prognostic significance of ceRNA interaction. RESULTS: Incorporating the knowledge that ceRNA interaction is highly condition-specific and modulated by the expressional abundance of miRNAs, we devised a ceRNA inference by differential correlation analysis to identify the miRNA-modulated ceRNA pairs. Analyzing sample-paired miRNA and gene expression profiles of GBM, our data showed that this alternative layer of gene interaction is essential in global information flow. Functional annotation analysis revealed its involvement in activated processes in brain, such as synaptic transmission, as well as critical tumor-associated functions. Notably, a systematic survival analysis suggested the strength of ceRNA-ceRNA interactions, rather than expressional abundance of individual ceRNAs, among three immune response genes (CCL22, IL2RB, and IRF4) is predictive of patient survival. The prognostic value was validated in two independent cohorts. CONCLUSIONS: This work addresses the lack of a comprehensive exploration into the functional and prognostic relevance of ceRNA interaction in GBM. The proposed efficient and reliable method revealed its significance in GBM-related functions and prognosis. The highlighted roles of ceRNA interaction provide a basis for further biological and clinical investigations.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/mortalidade
Glioblastoma/mortalidade
RNA Neoplásico/metabolismo
[Mh] Termos MeSH secundário: Neoplasias Encefálicas/genética
Neoplasias Encefálicas/metabolismo
Quimiocina CCL22/genética
Epistasia Genética
Glioblastoma/genética
Glioblastoma/metabolismo
Seres Humanos
Fatores Reguladores de Interferon/genética
Subunidade beta de Receptor de Interleucina-2/genética
MicroRNAs/metabolismo
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL22 protein, human); 0 (Chemokine CCL22); 0 (IL2RB protein, human); 0 (Interferon Regulatory Factors); 0 (Interleukin-2 Receptor beta Subunit); 0 (MicroRNAs); 0 (RNA, Neoplasm); 0 (interferon regulatory factor-4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170301
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-017-1557-4


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[PMID]:28178051
[Au] Autor:Abernethy MG; Rosenfeld A; White JR; Mueller MG; Lewicky-Gaupp C; Kenton K
[Ad] Endereço:Northwestern Feinberg School of Medicine, Chicago, Illinois; Columbia University, New York, New York; and Resphera Biosciences, Baltimore, Maryland.
[Ti] Título:Urinary Microbiome and Cytokine Levels in Women With Interstitial Cystitis.
[So] Source:Obstet Gynecol;129(3):500-506, 2017 Mar.
[Is] ISSN:1873-233X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate differences in the urinary microbiome and cytokine levels between women with and without interstitial cystitis and to correlate differences with scores on standardized symptom severity scales and depression and anxiety screening tools. METHODS: Our cross-sectional study compared women presenting to a pelvic floor clinic and diagnosed with interstitial cystitis over a 6-month period with age-matched women in a control group from the same institution. Participants provided a catheterized urine sample and completed symptom severity, quality-of-life, depression, and anxiety screening questionnaires. Urinary microbiomes generated through bacterial ribosomal RNA sequencing and cytokine levels were analyzed using a standard immunoassay. Nonparametric analyses were used for all comparisons. RESULTS: Participants with interstitial cystitis reported more disability, bothersome urinary symptoms, genitourinary pain, and sexual dysfunction and scored higher on depression and anxiety screens compared with women in the control group. The urine of participants with interstitial cystitis contained fewer distinct operational taxonomic units (2 [median range 2-7, interquartile range 1] compared with 3.5 [median, range 2-22, interquartile range 5.25], P=.015) and was less likely to contain Lactobacillus acidophilus (1/14 [7%] compared with 7/18 [39%], P=.05) compared with women in the control group. L acidophilus was associated with less severe scores on the Interstitial Cystitis Symptoms Index (1 [median, range 0-17, interquartile range 5] compared with 10 [median, range 0-14, interquartile range 11], P=.005) and the Genitourinary Pain Index (0 [median, range 0-42, interquartile range 22] compared with 22.5 [median, range 0-40, interquartile range 28], P=.03). Participants with interstitial cystitis demonstrated higher levels of macrophage-derived chemokine (13.32 [median, range 8.93-17.05, interquartile range 15.86] compared with 0 [median, range 8.93-22.67, interquartile range 10.35], P=.037) and interleukin-4 (1.95 [median, range 1.31-997, interquartile range 11.84] compared with 1.17 [median, range 0.44-3.26, interquartile range 1.51], P=.029). There was a positive correlation between interleukin-4 and more severe scores on the Interstitial Cystitis Symptoms Index (r=0.406, P=.013). No associations between the presence of lactobacillus species and cytokine levels were observed. CONCLUSION: The urinary microbiome of participants with interstitial cystitis was less diverse, less likely to contain Lactobacillus species, and associated with higher levels of proinflammatory cytokines. It is unknown whether this represents causality and whether the effect of alterations to the urinary microbiome is mediated through an inflammatory response.
[Mh] Termos MeSH primário: Quimiocina CCL22/sangue
Cistite Intersticial/sangue
Interleucina-4/sangue
Lactobacillus acidophilus/isolamento & purificação
Microbiota
Sistema Urinário/microbiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Estudos Transversais
Cistite Intersticial/complicações
Feminino
Seres Humanos
Meia-Idade
Dor/etiologia
Medição da Dor
Índice de Gravidade de Doença
Urina/microbiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL22 protein, human); 0 (Chemokine CCL22); 207137-56-2 (Interleukin-4)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170616
[Lr] Data última revisão:
170616
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1097/AOG.0000000000001892


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[PMID]:28108556
[Au] Autor:Molineros JE; Yang W; Zhou XJ; Sun C; Okada Y; Zhang H; Heng Chua K; Lau YL; Kochi Y; Suzuki A; Yamamoto K; Ma J; Bang SY; Lee HS; Kim K; Bae SC; Zhang H; Shen N; Looger LL; Nath SK
[Ad] Endereço:Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.
[Ti] Título:Confirmation of five novel susceptibility loci for systemic lupus erythematosus (SLE) and integrated network analysis of 82 SLE susceptibility loci.
[So] Source:Hum Mol Genet;26(6):1205-1216, 2017 Mar 15.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We recently identified ten novel SLE susceptibility loci in Asians and uncovered several additional suggestive loci requiring further validation. This study aimed to replicate five of these suggestive loci in a Han Chinese cohort from Hong Kong, followed by meta-analysis (11,656 cases and 23,968 controls) on previously reported Asian and European populations, and to perform bioinformatic analyses on all 82 reported SLE loci to identify shared regulatory signatures. We performed a battery of analyses for these five loci, as well as joint analyses on all 82 SLE loci. All five loci passed genome-wide significance: MYNN (rs10936599, Pmeta = 1.92 × 10-13, OR = 1.14), ATG16L2 (rs11235604, Pmeta = 8.87 × 10 -12, OR = 0.78), CCL22 (rs223881, Pmeta = 5.87 × 10-16, OR = 0.87), ANKS1A (rs2762340, Pmeta = 4.93 × 10-15, OR = 0.87) and RNASEH2C (rs1308020, Pmeta = 2.96 × 10-19, OR = 0.84) and co-located with annotated gene regulatory elements. The novel loci share genetic signatures with other reported SLE loci, including effects on gene expression, transcription factor binding, and epigenetic characteristics. Most (56%) of the correlated (r2 > 0.8) SNPs from the 82 SLE loci were implicated in differential expression (9.81 × 10-198 < P < 5 × 10-3) of cis-genes. Transcription factor binding sites for p53, MEF2A and E2F1 were significantly (P < 0.05) over-represented in SLE loci, consistent with apoptosis playing a critical role in SLE. Enrichment analysis revealed common pathways, gene ontology, protein domains, and cell type-specific expression. In summary, we provide evidence of five novel SLE susceptibility loci. Integrated bioinformatics using all 82 loci revealed that SLE susceptibility loci share many gene regulatory features, suggestive of conserved mechanisms of SLE etiopathogenesis.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Lúpus Eritematoso Sistêmico/genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Grupo com Ancestrais do Continente Asiático
Proteínas Relacionadas à Autofagia/genética
Quimiocina CCL22/genética
Regulação da Expressão Gênica/genética
Genótipo
Seres Humanos
Fatores de Transcrição Kruppel-Like/genética
Lúpus Eritematoso Sistêmico/epidemiologia
Lúpus Eritematoso Sistêmico/patologia
Polimorfismo de Nucleotídeo Único/genética
Ribonuclease H/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATG16L1 protein, human); 0 (Adaptor Proteins, Signal Transducing); 0 (Autophagy-Related Proteins); 0 (CCL22 protein, human); 0 (Chemokine CCL22); 0 (Kruppel-Like Transcription Factors); 0 (MYNN protein, human); 0 (Odin protein, human); EC 3.1.26.- (ribonuclease HII); EC 3.1.26.4 (Ribonuclease H)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170122
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx026


  8 / 456 MEDLINE  
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[PMID]:27846260
[Au] Autor:Soldano S; Pizzorni C; Paolino S; Trombetta AC; Montagna P; Brizzolara R; Ruaro B; Sulli A; Cutolo M
[Ad] Endereço:Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, Genoa, Italy.
[Ti] Título:Alternatively Activated (M2) Macrophage Phenotype Is Inducible by Endothelin-1 in Cultured Human Macrophages.
[So] Source:PLoS One;11(11):e0166433, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Alternatively activated (M2) macrophages are phenotypically characterized by the expression of specific markers, mainly macrophage scavenger receptors (CD204 and CD163) and mannose receptor-1 (CD206), and participate in the fibrotic process by over-producing pro-fibrotic molecules, such as transforming growth factor-beta1 (TGFbeta1) and metalloproteinase (MMP)-9. Endothelin-1 (ET-1) is implicated in the fibrotic process, exerting its pro-fibrotic effects through the interaction with its receptors (ETA and ETB). The study investigated the possible role of ET-1 in inducing the transition from cultured human macrophages into M2 cells. METHODS: Cultured human monocytes (THP-1 cell line) were activated into macrophages (M0 macrophages) with phorbol myristate acetate and subsequently maintained in growth medium (M0-controls) or treated with either ET-1 (100nM) or interleukin-4 (IL-4, 10ng/mL, M2 inducer) for 72 hours. Similarly, primary cultures of human peripheral blood monocyte (PBM)-derived macrophages obtained from healthy subjects, were maintained in growth medium (untreated cells) or treated with ET-1 or IL-4 for 6 days. Both M0 and PBM-derived macrophages were pre-treated with ET receptor antagonist (ETA/BRA, bosentan 10-5M) for 1 hour before ET-1 stimulation. Protein and gene expression of CD204, CD206, CD163, TGFbeta1 were analysed by immunocytochemistry, Western blotting and quantitative real time polymerase chain reaction (qRT-PCR). Gene expression of interleukin(IL)-10 and macrophage derived chemokine (CCL-22) was evaluated by qRT-PCR. MMP-9 production was investigated by gel zymography. RESULTS: ET-1 significantly increased the expression of M2 phenotype markers CD204, CD206, CD163, IL-10 and CCL-22, and the production of MMP-9 in both cultures of M0 and PBM-derived macrophages compared to M0-controls and untreated cells. In cultured PBM-derived macrophages, ET-1 increased TGFbeta1 protein and gene expression compared to untreated cells. The ET-1-mediated effects were contrasted by ETA/BRA treatment in both cultured cell types. CONCLUSION: ET-1 seems to induce the M2 phenotype in cultured human macrophages, a process apparently contrasted by the action of the ETA/BRA, suggesting possible clinical implications in those fibrotic diseases characterized by increased ET-1 concentrations, such as systemic sclerosis but also type 2 diabetes.
[Mh] Termos MeSH primário: Endotelina-1/farmacologia
Ativação de Macrófagos/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Monócitos/efeitos dos fármacos
Receptor de Endotelina A/genética
[Mh] Termos MeSH secundário: Antígenos CD/genética
Antígenos CD/imunologia
Antígenos de Diferenciação Mielomonocítica/genética
Antígenos de Diferenciação Mielomonocítica/imunologia
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Quimiocina CCL22/genética
Quimiocina CCL22/imunologia
Antagonistas dos Receptores de Endotelina/farmacologia
Regulação da Expressão Gênica
Seres Humanos
Interleucina-10/genética
Interleucina-10/imunologia
Interleucina-4/farmacologia
Lectinas Tipo C/genética
Lectinas Tipo C/imunologia
Macrófagos/citologia
Macrófagos/imunologia
Lectinas de Ligação a Manose/genética
Lectinas de Ligação a Manose/imunologia
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/imunologia
Monócitos/citologia
Monócitos/imunologia
Fenótipo
Cultura Primária de Células
Receptor de Endotelina A/imunologia
Receptores de Superfície Celular/genética
Receptores de Superfície Celular/imunologia
Receptores Depuradores Classe A/genética
Receptores Depuradores Classe A/imunologia
Sulfonamidas/farmacologia
Acetato de Tetradecanoilforbol/farmacologia
Fator de Crescimento Transformador beta1/genética
Fator de Crescimento Transformador beta1/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CCL22 protein, human); 0 (CD163 antigen); 0 (Chemokine CCL22); 0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (IL10 protein, human); 0 (IL4 protein, human); 0 (Lectins, C-Type); 0 (MSR1 protein, human); 0 (Mannose-Binding Lectins); 0 (Receptor, Endothelin A); 0 (Receptors, Cell Surface); 0 (Scavenger Receptors, Class A); 0 (Sulfonamides); 0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); 0 (mannose receptor); 130068-27-8 (Interleukin-10); 207137-56-2 (Interleukin-4); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9); NI40JAQ945 (Tetradecanoylphorbol Acetate); Q326023R30 (bosentan)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0166433


  9 / 456 MEDLINE  
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[PMID]:27825407
[Au] Autor:Zhao MY; Zhao J; Yang T; Wang L; Pei ML; Tian SJ; Yu Y; Yang XF
[Ad] Endereço:Department of Obstetrics and Gynecology,the First Affiliated Hospital, Xi'an Jiaotong University,Xi'an 710061,China.
[Ti] Título:Aberrant Expressions of Immune Factors Facilitate the Disequilibrium of Immune Status in Cervical Cancer.
[So] Source:Zhongguo Yi Xue Ke Xue Yuan Xue Bao;38(5):522-527, 2016 10 10.
[Is] ISSN:1000-503X
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Objective To explore the expressions and co-relationship of immune factors forkhead box p3 (FoxP3),chemokine (C-C motif) ligand 22 (CCL22),tumor necrosis factor receptor superfamily member 40(OX40),and SMAD family member 3 (Smad3) in cervical carcinoma and investigate their immunomodulatory roles in cervical carcinogenesis.Methods Totally 30 cases of cervical carcinoma with adjacent tissues and 20 cases of normal cervix were collected in this study. FoxP3,CCL22,OX40,and Smad3 mRNA expressions were detected by real-time polymerase chain reaction (RT-PCR). Results Compared to normal cervix,the expression levels of FoxP3 and CCL22 mRNA were elevated in neoplastic foci(P=0.000,P=0.002) and tumor periphery (P=0.048,P=0.040).The mRNAs increased modestly in high-grade squamous cell carcinoma focal(P=0.019,P=0.020) and periphery tissue (P=0.023,P=0.031) in comparison with low-grade squamous cell carcinoma. The expression levels of OX40 and Smad3 mRNA were significantly lower in neoplastic foci(P=0.000,P=0.015) than normal cervix. Compared to low-grade squamous cell carcinoma focal and periphery tissue,the mRNAs decreased moderately in high-grade squamous cell carcinoma(P=0.018,P=0.030; P=0.027,P=0.014). In both neoplastic foci and tumor periphery,the mRNA expression level of CCL22 was positively correlated with FoxP3 (r=0.353,P=0.000; r=0.307,P=0.000) but negatively correlated with OX40 (r=-0.288,P=0.031; r=-0.263,P=0.037),while OX40 was positively correlated with Smad3 (r=0.384,P=0.002;r=0.288,P=0.023). The mRNA expressions of FoxP3 and CCL22 were increased in foci and pericarcinous tissues (P=0.024,P=0.039; P=0.032,P=0.034) while Smad3 was decreased in neoplastic foci (P=0.017) in contrast to HPV negative corresponding group. Conclusion FoxP3 and CCL22 expressions increase while OX40 and Smad3 expression decrease at mRNA level in the microenvironment of cervical cancer,which may be associated with such immunological model that the immunosuppressive roles of FoxP3 and CCL22 enhance while the immunity-boosting roles of OX40 and Smad3 are impeded,contributing to the deterioration of immune disequilibrium in local site and cervical cancer carcinogenesis.
[Mh] Termos MeSH primário: Quimiocina CCL22/metabolismo
Fatores de Transcrição Forkhead/metabolismo
Receptores OX40/metabolismo
Proteína Smad3/metabolismo
Neoplasias do Colo do Útero/imunologia
[Mh] Termos MeSH secundário: Carcinoma de Células Escamosas/imunologia
Feminino
Seres Humanos
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL22 protein, human); 0 (Chemokine CCL22); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (RNA, Messenger); 0 (Receptors, OX40); 0 (SMAD3 protein, human); 0 (Smad3 Protein); 0 (TNFRSF4 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161110
[St] Status:MEDLINE
[do] DOI:10.3881/j.issn.1000-503X.2016.05.005


  10 / 456 MEDLINE  
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[PMID]:27696405
[Au] Autor:Lim SJ; Kim M; Randy A; Nam EJ; Nho CW
[Ad] Endereço:Natural Products Research Center, Korea Institute of Science and Technology, Gangneung, Korea.
[Ti] Título:Effects of Hovenia dulcis Thunb. extract and methyl vanillate on atopic dermatitis-like skin lesions and TNF-α/IFN-γ-induced chemokines production in HaCaT cells.
[So] Source:J Pharm Pharmacol;68(11):1465-1479, 2016 Nov.
[Is] ISSN:2042-7158
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Here, we hypothesized that Hovenia dulcis branch extract (HDB) and its active constituents ameliorates 2,4-dinitrochlorobenzene-induced atopic dermatitis (AD)-like skin lesions by modulating the T helper Th1/Th2 balance in NC/Nga mice and TNF-α- and IFN-γ-induced production of thymus and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC) in HaCaT cells. METHODS: HaCaT cells were stimulated by TNF-α/IFN-γ in the presence of HDB and its constituents. TARC and MDC were measured by ELISA and RT-PCR. For the in-vivo study, oral feeding of HDB was performed for 5 weeks with 2,4-dinitrochlorobenzene (DNCB) treatment every other day. The efficacy of HDB on parameters of DNCB-induced AD was evaluated morphologically, physiologically and immunologically. KEY FINDINGS: In-vitro studies showed that HDB and its constituents suppressed TNF-α/IFN-γ-induced production of TARC and MDC in HaCaT cells by inhibiting MAPK signalling. In-vivo studies showed that HDB regulated immunoglobulin (Ig) E and immunoglobulin G2a (IgG2a) levels in serum and the expression of mRNA for Th1- and Th2-related mediators in skin lesions. Histopathological analyses revealed reduced epidermal thickness and reduced infiltration of skin lesions by inflammatory cells. CONCLUSION: These results suggest that HDB inhibits AD-like skin diseases by regulating Th1 and Th2 responses in NC/Nga mice and in HaCaT cells.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Quimiocinas/metabolismo
Dermatite Atópica/prevenção & controle
Queratinócitos/efeitos dos fármacos
Extratos Vegetais/farmacologia
Rhamnaceae/química
Pele/efeitos dos fármacos
Ácido Vanílico/análogos & derivados
Ácido Vanílico/farmacologia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/isolamento & purificação
Linhagem Celular
Quimiocina CCL17/metabolismo
Quimiocina CCL22/metabolismo
Quimiocinas/sangue
Quimiocinas/imunologia
Dermatite Atópica/sangue
Dermatite Atópica/induzido quimicamente
Dermatite Atópica/imunologia
Dinitroclorobenzeno
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Seres Humanos
Imunoglobulina E/sangue
Imunoglobulina G/sangue
Interferon gama/farmacologia
Queratinócitos/imunologia
Queratinócitos/metabolismo
Masculino
Camundongos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fitoterapia
Extratos Vegetais/isolamento & purificação
Plantas Medicinais
Transdução de Sinais/efeitos dos fármacos
Pele/imunologia
Pele/metabolismo
Pele/patologia
Células Th1/efeitos dos fármacos
Células Th1/imunologia
Células Th1/metabolismo
Equilíbrio Th1-Th2/efeitos dos fármacos
Células Th2/efeitos dos fármacos
Células Th2/imunologia
Células Th2/metabolismo
Fatores de Transcrição/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
Ácido Vanílico/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (CCL17 protein, human); 0 (CCL22 protein, human); 0 (Chemokine CCL17); 0 (Chemokine CCL22); 0 (Chemokines); 0 (Immunoglobulin G); 0 (Plant Extracts); 0 (Transcription Factors); 0 (Tumor Necrosis Factor-alpha); 0 (methyl vanillate); 37341-29-0 (Immunoglobulin E); 82115-62-6 (Interferon-gamma); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); GE3IBT7BMN (Dinitrochlorobenzene); GM8Q3JM2Y8 (Vanillic Acid)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE
[do] DOI:10.1111/jphp.12640



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