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Pesquisa : D12.644.276.374.200.120.250 [Categoria DeCS]
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[PMID]:29346400
[Au] Autor:Ponert JM; Schwarz S; Haschemi R; Müller J; Pötzsch B; Bendas G; Schlesinger M
[Ad] Endereço:Department of Pharmacy, Rheinische Friedrich-Wilhelms-University Bonn, Bonn, Germany.
[Ti] Título:The mechanisms how heparin affects the tumor cell induced VEGF and chemokine release from platelets to attenuate the early metastatic niche formation.
[So] Source:PLoS One;13(1):e0191303, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metastasis is responsible for the majority of cancer associated fatalities. Tumor cells leaving the primary tumor and entering the blood flow immediately interact with platelets. Activated platelets contribute in different ways to cancer cell survival and proliferation, e.g. in formation of the early metastatic niche by release of different growth factors and chemokines. Here we show that a direct interaction between platelets and MV3 melanoma or MCF7 breast cancer cells induces platelet activation and a VEGF release in citrated plasma that cannot be further elevated by the coagulation cascade and generated thrombin. In contrast, the release of platelet-derived chemokines CXCL5 and CXCL7 depends on both, a thrombin-mediated platelet activation and a direct interaction between tumor cells and platelets. Preincubation of platelets with therapeutic concentrations of unfractionated heparin reduces the tumor cell initiated VEGF release from platelets. In contrast, tumor cell induced CXCL5 and CXCL7 release from platelets was not impacted by heparin pretreatment in citrated plasma. In defibrinated, recalcified plasma, on the contrary, heparin is able to reduce CXCL5 and CXCL7 release from platelets by thrombin inhibition. Our data indicate that different chemokines and growth factors in diverse platelet granules are released in tightly regulated processes by various trigger mechanisms. We show for the first time that heparin is able to reduce the mediator release induced by different tumor cells both in a contact and coagulation dependent manner.
[Mh] Termos MeSH primário: Plaquetas/efeitos dos fármacos
Quimiocina CXCL5/secreção
Heparina/farmacologia
Microambiente Tumoral/efeitos dos fármacos
Fator A de Crescimento do Endotélio Vascular/secreção
beta-Tromboglobulina/secreção
[Mh] Termos MeSH secundário: Coagulação Sanguínea/efeitos dos fármacos
Plaquetas/fisiologia
Linhagem Celular Tumoral
Seres Humanos
Metástase Neoplásica
Ativação Plaquetária/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CXCL5); 0 (PPBP protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (beta-Thromboglobulin); 9005-49-6 (Heparin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191303


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[PMID]:28916286
[Au] Autor:Pénzes Á; Mahmud Abdelwahab EM; Rapp J; Péteri ZA; Bovári-Biri J; Fekete C; Miskei G; Kvell K; Pongrácz JE
[Ad] Endereço:PannonPharma Ltd., Biological Control Laboratory, 1 Pannonpharma Str., H-7720, Pécsvárad, Hungary.
[Ti] Título:Toxicology studies of primycin-sulphate using a three-dimensional (3D) in vitro human liver aggregate model.
[So] Source:Toxicol Lett;281:44-52, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Primycin-sulphate is a highly effective compound against Gram (G) positive bacteria. It has a potentially synergistic effect with vancomycin and statins which makes primycin-sulphate a potentially very effective preparation. Primycin-sulphate is currently used exclusively in topical preparations. In vitro animal hepatocyte and neuromuscular junction studies (in mice, rats, snakes, frogs) as well as in in vitro human red blood cell experiments were used to test toxicity. During these studies, the use of primycin-sulphate resulted in reduced cellular membrane integrity and modified ion channel activity. Additionally, parenteral administration of primycin-sulphate to mice, dogs, cats, rabbits and guinea pigs indicated high level of acute toxicity. The objective of this study was to reveal the cytotoxic and gene expression modifying effects of primycin-sulphate in a human system using an in vitro, three dimensional (3D) human hepatic model system. Within the 3D model, primycin-sulphate presented no acute cytotoxicity at concentrations 1µg/ml and below. However, even at low concentrations, primycin-sulphate affected gene expressions by up-regulating inflammatory cytokines (e.g., IL6), chemokines (e.g., CXCL5) and by down-regulating molecules of the lipid metabolism (e.g., peroxisome proliferator receptor (PPAR) alpha, gamma, etc). Down-regulation of PPAR alpha cannot just disrupt lipid production but can also affect cytochrome P450 metabolic enzyme (CYP) 3A4 expression, highlighting the need for extensive drug-drug interaction (DDI) studies before human oral or parenteral preparations can be developed.
[Mh] Termos MeSH primário: Imagem Tridimensional
Macrolídeos/toxicidade
Sulfatos/toxicidade
[Mh] Termos MeSH secundário: Sobrevivência Celular/efeitos dos fármacos
Quimiocina CXCL5/genética
Quimiocina CXCL5/metabolismo
Técnicas de Cocultura
Citocromo P-450 CYP3A/genética
Citocromo P-450 CYP3A/metabolismo
Relação Dose-Resposta a Droga
Regulação para Baixo
Determinação de Ponto Final
Células Hep G2
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Seres Humanos
Interleucina-6/genética
Interleucina-6/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Análise em Microsséries
Modelos Moleculares
PPAR alfa/genética
PPAR alfa/metabolismo
PPAR gama/genética
PPAR gama/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL5 protein, human); 0 (Chemokine CXCL5); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Macrolides); 0 (PPAR alpha); 0 (PPAR gamma); 0 (Sulfates); EC 1.14.13.67 (CYP3A4 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP3A); M3Y14N50DX (primycin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE


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[PMID]:28545284
[Au] Autor:Fan FD; Xu ZJ; Zhou Q; Wang DJ
[Ad] Endereço:Department of Cardiothoracic Surgery, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, China.
[Ti] Título:[Expression profiles and clinical implication of plasma chemokines in patients with Stanford type A aortic dissection].
[So] Source:Zhonghua Xin Xue Guan Bing Za Zhi;45(4):318-322, 2017 Apr 24.
[Is] ISSN:0253-3758
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the plasma chemokines expressions and related clinical implication in patients with Stanford type A aortic dissection (AD). We retrospectively analyzed the data of 65 patients with Stanford type A aortic dissection, hypertensive patients and 11 healthy subjects admitted in our department from October 2013 to December 2014, they were divided into four groups: NH-CON group (11 healthy subjects), H-AD group (29 AD patients with hypertension), NH-AD group (21 AD patients without hypertension), and H-CON group (14 hypertension patients). Four plasma samples from AD patients and 4 plasma samples from healthy subjects were collected randomly with random numbers table, and the levels of different chemokines were examined by protein array analysis. Then, plasma levels of chemokines including macrophage inflammatory protein 1ß(MIP-1ß), epithelial neutrophil activating peptide 78(ENA-78), interleukin 16(IL-16), interferon inducible protein 10(IP-10) and FMS-like tyrosine kinase 3(Flt-3) ligand were analyzed by luminex. Pearson analysis was used to determine the correlations between the chemokines and serum C reactive protein (CRP) levels. Plasma levels of MIP-1ß(34.0(29.3, 47.2) ng/L vs. 51.0(28.2, 80.7) ng/L, <0.05) and ENA-78(110.5(59.1, 161.4) ng/L vs. 475.7(299.3, 837.3) ng/L, <0.05) were significantly lower in H-AD group, while plasma IL-16 level was significantly higher in H-AD group(54.7(16.3, 187.8) ng/L vs. 17.5(11.9, 20.8) ng/L, <0.05) than in H-CON group. Plasma levels of MIP-1ß(48.3(26.4, 62.1) ng/L, <0.05) were significantly lower in H-AD patients than in NH-AD patients. Plasma level of ENA-78 was significantly lower in NH-AD group than in NH-CON group (95.0(58.0, 155.0) ng/L vs. 257.7(85.2, 397.8) ng/L, <0.05). The levels of IP-10 and Flt-3 ligand were similar among the 4 groups (all >0.05). Pearson analysis showed that there were no correlation between MIP-1ß( (2)=0.01, >0.05), ENA-78( (2)=0.02, >0.05), IL-16( (2)=0.02, >0.05), IP-10( (2)=0.00, >0.05), Flt-3 ligand( (2)=0.02, >0.05) and CRP levels in patients with Stanford type A aortic dissection. Lower plasma levels of MIP-1ß and ENA-78 and higher plasma levels of IL-16 may associate with the occurrence and development of type A aortic dissection, but their concentrations are not correlated with serum CRP levels. There is no significant change on plasma levels of IP-10 and Flt-3 in the Stanford type A aortic dissection patients.
[Mh] Termos MeSH primário: Aneurisma da Aorta Torácica
Quimiocina CCL4
Tirosina Quinase 3 Semelhante a fms
[Mh] Termos MeSH secundário: Aneurisma Dissecante
Estudos de Casos e Controles
Quimiocina CXCL5
Quimiocinas
Seres Humanos
Hipertensão
Proteínas de Membrana
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL4 protein, human); 0 (CXCL5 protein, human); 0 (Chemokine CCL4); 0 (Chemokine CXCL5); 0 (Chemokines); 0 (Membrane Proteins); 0 (flt3 ligand protein); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3758.2017.04.012


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[PMID]:28522730
[Au] Autor:Mylonas KJ; Turner NA; Bageghni SA; Kenyon CJ; White CI; McGregor K; Kimmitt RA; Sulston R; Kelly V; Walker BR; Porter KE; Chapman KE; Gray GA
[Ad] Endereço:University/BHF Centre for Cardiovascular ScienceUniversity of Edinburgh, Queen's Medical Research Institute, Edinburgh, UK.
[Ti] Título:11ß-HSD1 suppresses cardiac fibroblast CXCL2, CXCL5 and neutrophil recruitment to the heart post MI.
[So] Source:J Endocrinol;233(3):315-327, 2017 Jun.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We have previously demonstrated that neutrophil recruitment to the heart following myocardial infarction (MI) is enhanced in mice lacking 11ß-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) that regenerates active glucocorticoid within cells from intrinsically inert metabolites. The present study aimed to identify the mechanism of regulation. In a mouse model of MI, neutrophil mobilization to blood and recruitment to the heart were higher in 11ß-HSD1-deficient ( ) relative to wild-type (WT) mice, despite similar initial injury and circulating glucocorticoid. In bone marrow chimeric mice, neutrophil mobilization was increased when 11ß-HSD1 was absent from host cells, but not when absent from donor bone marrow-derived cells. Consistent with a role for 11ß-HSD1 in 'host' myocardium, gene expression of a subset of neutrophil chemoattractants, including the chemokines and , was selectively increased in the myocardium of mice relative to WT. SM22α-Cre directed disruption of in smooth muscle and cardiomyocytes had no effect on neutrophil recruitment. Expression of and was elevated in fibroblast fractions isolated from hearts of mice post MI and provision of either corticosterone or of the 11ß-HSD1 substrate, 11-dehydrocorticosterone, to cultured murine cardiac fibroblasts suppressed IL-1α-induced expression of and These data identify suppression of CXCL2 and CXCL5 chemoattractant expression by 11ß-HSD1 as a novel mechanism with potential for regulation of neutrophil recruitment to the injured myocardium, and cardiac fibroblasts as a key site for intracellular glucocorticoid regeneration during acute inflammation following myocardial injury.
[Mh] Termos MeSH primário: 11-beta-Hidroxiesteroide Desidrogenase Tipo 1/metabolismo
Quimiocina CXCL2/metabolismo
Quimiocina CXCL5/metabolismo
Fibroblastos/fisiologia
Neutrófilos/fisiologia
[Mh] Termos MeSH secundário: 11-beta-Hidroxiesteroide Desidrogenase Tipo 1/genética
Animais
Células da Medula Óssea
Células Cultivadas
Quimiocina CXCL5/genética
Corticosterona/análogos & derivados
Corticosterona/farmacologia
Masculino
Camundongos
Camundongos Knockout
Proteínas dos Microfilamentos/genética
Proteínas dos Microfilamentos/metabolismo
Proteínas Musculares/genética
Proteínas Musculares/metabolismo
Infarto do Miocárdio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL2); 0 (Chemokine CXCL5); 0 (Microfilament Proteins); 0 (Muscle Proteins); 0 (transgelin); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenase Type 1); FO4V44A3G3 (11-dehydrocorticosterone); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-16-0501


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[PMID]:28356111
[Au] Autor:Zhao J; Ou B; Han D; Wang P; Zong Y; Zhu C; Liu D; Zheng M; Sun J; Feng H; Lu A
[Ad] Endereço:Shanghai Minimally Invasive Surgery Center, Ruijin hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
[Ti] Título:Tumor-derived CXCL5 promotes human colorectal cancer metastasis through activation of the ERK/Elk-1/Snail and AKT/GSK3ß/ß-catenin pathways.
[So] Source:Mol Cancer;16(1):70, 2017 Mar 29.
[Is] ISSN:1476-4598
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Metastasis is a major cause of death in human colorectal cancer patients. However, the contribution of chemokines in the tumor microenvironment to tumor metastasis is not fully understood. METHODS: Herein, we examinined several chemokines in colorectal cancer patients using chemokine ELISA array. Immunohistochemistry was used to detect expression of CXCL5 in colorectal cancer patients tissues. Human HCT116 and SW480 cell lines stably transfected with CXCL5, shCXCL5 and shCXCR2 lentivirus plasmids were used in our in vitro study. Immunoblot, immunofluorescence and transwell assay were used to examine the molecular biology and morphological changes in these cells. In addition, we used nude mice to detect the influence of CXCL5 on tumor metastasis in vivo. RESULTS: We found that CXCL5 was overexpressed in tumor tissues and associated with advanced tumor stage as well as poor prognosis in colorectal cancer patients. We also demonstrated that CXCL5 was primarily expressed in the tumor cell cytoplasm and cell membranes, which may indicate that the CXCL5 was predominantly produced by cancer epithelial cells instead of fibroblasts in the tumor mesenchyme. Additionally, overexpression of CXCL5 enhanced the migration and invasion of colorectal cancer cells by inducing the epithelial-mesenchymal transition (EMT) through activation of the ERK/Elk-1/Snail pathway and the AKT/GSK3ß/ß-catenin pathway in a CXCR2-dependent manner. The silencing of Snail and ß-catenin attenuated CXCL5/CXCR2-enhanced cell migration and invasion in vitro. The elevated expression of CXCL5 can also potentiate the metastasis of colorectal cancer cells to the liver in vivo in nude mice intrasplenic injection model. CONCLUSION: In conclusion, our findings support CXCL5 as a promoter of colorectal cancer metastasis and a predictor of poor clinical outcomes in colorectal cancer patients.
[Mh] Termos MeSH primário: Quimiocina CXCL5/metabolismo
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Quimiocina CXCL5/genética
Análise por Conglomerados
Neoplasias Colorretais/genética
Modelos Animais de Doenças
Transição Epitelial-Mesenquimal
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Perfilação da Expressão Gênica
Glicogênio Sintase Quinase 3 beta/metabolismo
Xenoenxertos
Seres Humanos
Neoplasias Hepáticas/secundário
Camundongos
Modelos Biológicos
Prognóstico
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de Interleucina-8B/metabolismo
Fatores de Transcrição da Família Snail/metabolismo
beta Catenina/metabolismo
Proteínas Elk-1 do Domínio ets/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL5); 0 (Receptors, Interleukin-8B); 0 (Snail Family Transcription Factors); 0 (beta Catenin); 0 (ets-Domain Protein Elk-1); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1186/s12943-017-0629-4


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[PMID]:28277189
[Au] Autor:Dang H; Wu W; Wang B; Cui C; Niu J; Chen J; Chen Z; Liu Y
[Ad] Endereço:Department of Orthopaedics, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, P.R. China.
[Ti] Título:CXCL5 Plays a Promoting Role in Osteosarcoma Cell Migration and Invasion in Autocrine- and Paracrine-Dependent Manners.
[So] Source:Oncol Res;25(2):177-186, 2017 Jan 26.
[Is] ISSN:1555-3906
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CXCL5, a CXC-type chemokine, is an important attractant for granulocytic immune cells by binding to its receptor CXCR2. Recently, CXCL5/CXCR2 has been found to play an oncogenic role in many human cancers. However, the exact role of CXCL5 in osteosarcoma cell migration and invasion has not been revealed. Here we found that the protein expression of CXCL5 was significantly increased in osteosarcoma tissues compared with that in matched adjacent nontumor tissues. Moreover, the expression of CXCL5 was significantly associated with advanced clinical stage and metastasis. Further investigation showed that the CXCL5 expression levels were also significantly increased in osteosarcoma cell lines, including Saos-2, MG63, U2OS, and SW1353, when compared with those in normal osteoblast hFoB1.19 cells. U2OS cells were further transfected with CXCL5-specific siRNA or overexpression plasmid. Knockdown of CXCL5 significantly suppressed U2OS cell migration and invasion. On the contrary, overexpression of CXLC5 remarkably promoted the migration and invasion of U2OS cells. Interestingly, both exogenous CXCL5 treatment and the conditioned medium of CXCL5-overexpressing hFoB1.19 cells could also enhance the migration and invasion of U2OS cells, suggesting that the promoting role of CXCL5 in U2OS cell migration and invasion is also in a paracrine-dependent manner. According to these data, our study demonstrates that CXCL5 is upregulated in osteosarcoma and may play an oncogenic role in osteosarcoma metastasis. Therefore, CXCL5 may become a potential therapeutic target for osteosarcoma treatment.
[Mh] Termos MeSH primário: Comunicação Autócrina/fisiologia
Movimento Celular/fisiologia
Quimiocina CXCL5/fisiologia
Invasividade Neoplásica/patologia
Osteossarcoma/patologia
Comunicação Parácrina/fisiologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
Osteossarcoma/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL5 protein, human); 0 (Chemokine CXCL5)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170316
[Lr] Data última revisão:
170316
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.3727/096504016X14732772150343


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[PMID]:28053238
[Au] Autor:Chen W; Lu X; Chen Y; Li M; Mo P; Tong Z; Wang W; Wan W; Su G; Xu J; Yu C
[Ad] Endereço:State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen 361102, China.
[Ti] Título:Steroid Receptor Coactivator 3 Contributes to Host Defense against Enteric Bacteria by Recruiting Neutrophils via Upregulation of CXCL2 Expression.
[So] Source:J Immunol;198(4):1606-1615, 2017 Feb 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Steroid receptor coactivator 3 (SRC-3) is a transcriptional coactivator that interacts with nuclear receptors and some other transcription factors to enhance their effects on target gene transcription. We reported previously that SRC-3-deficient (SRC-3 ) mice are extremely susceptible to Escherichia coli-induced septic peritonitis as a result of uncontrolled inflammation and a defect in bacterial clearance. In this study, we observed significant upregulation of SRC-3 in colonic epithelial cells in response to Citrobacter rodentium infection. Based on these findings, we hypothesized that SRC-3 is involved in host defense against attaching and effacing bacterial infection. We compared the responses of SRC-3 and wild-type mice to intestinal C. rodentium infection. We found that SRC-3 mice exhibited delayed clearance of C. rodentium and more severe tissue pathology after oral infection with C. rodentium compared with wild-type mice. SRC-3 mice expressed normal antimicrobial peptides in the colons but exhibited delayed recruitment of neutrophils into the colonic mucosa. Accordingly, SRC-3 mice showed a delayed induction of CXCL2 and CXCL5 in colonic epithelial cells, which are responsible for neutrophil recruitment. At the molecular level, we found that SRC-3 can activate the NF-κB signaling pathway to promote CXCL2 expression at the transcriptional level. Collectively, we show that SRC-3 contributes to host defense against enteric bacteria, at least in part via upregulating CXCL2 expression to recruit neutrophils.
[Mh] Termos MeSH primário: Quimiocina CXCL2/genética
Infecções por Enterobacteriaceae/imunologia
Infiltração de Neutrófilos
Coativador 3 de Receptor Nuclear/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Peptídeos Catiônicos Antimicrobianos/genética
Peptídeos Catiônicos Antimicrobianos/imunologia
Quimiocina CXCL2/imunologia
Quimiocina CXCL5/genética
Quimiocina CXCL5/imunologia
Citrobacter rodentium/imunologia
Colite/microbiologia
Colite/patologia
Colo/imunologia
Colo/patologia
Interações Hospedeiro-Patógeno/imunologia
Inflamação
Mucosa Intestinal/imunologia
Mucosa Intestinal/microbiologia
Mucosa Intestinal/patologia
Camundongos
Camundongos Endogâmicos C57BL
NF-kappa B/metabolismo
Infiltração de Neutrófilos/imunologia
Coativador 3 de Receptor Nuclear/deficiência
Coativador 3 de Receptor Nuclear/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (Chemokine CXCL2); 0 (Chemokine CXCL5); 0 (Cxcl2 protein, mouse); 0 (Cxcl5 protein, mouse); 0 (NF-kappa B); EC 2.3.1.48 (Nuclear Receptor Coactivator 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600300


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[PMID]:27913793
[Au] Autor:Tran CT; Garcia M; Garnier M; Burucoa C; Bodet C
[Ad] Endereço:1 Laboratoire Inflammation, Tissus Epithéliaux et Cytokines (LITEC - EA 4331), Université de Poitiers, Poitiers, France.
[Ti] Título:Inflammatory signaling pathways induced by Helicobacter pylori in primary human gastric epithelial cells.
[So] Source:Innate Immun;23(2):165-174, 2017 Feb.
[Is] ISSN:1753-4267
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory signaling pathways induced by Helicobacter pylori remain unclear, having been studied mostly on cell-line models derived from gastric adenocarcinoma with potentially altered signaling pathways and nonfunctional receptors. Here, H. pylori-induced signaling pathways were investigated in primary human gastric epithelial cells. Inflammatory response was analyzed on chemokine mRNA expression and production after infection of gastric epithelial cells by H. pylori strains, B128 and B128Δ cagM, a cag type IV secretion system defective strain. Signaling pathway involvement was investigated using inhibitors of epidermal growth factor receptor (EGFR), MAPK, JAK and blocking Abs against TLR2 and TLR4. Inhibitors of EGFR, MAPK and JAK significantly reduced the chemokine mRNA expression and production induced by both H. pylori strains at 3 h and 24 h post-infection. JNK inhibitor reduced chemokine production at 24 h post-infection. Blocking Abs against TLR2 but not TLR4 showed significant reduction of chemokine secretion. Using primary culture of human gastric epithelial cells, our data suggest that H. pylori can be recognized by TLR2, leading to chemokine induction, and that EGFR, MAPK and the JAK/STAT signaling pathways play a key role in the H. pylori-induced CXCL1, CXCL5 and CXCL8 response in a cag pathogenicity island-independent manner.
[Mh] Termos MeSH primário: Células Epiteliais/imunologia
Infecções por Helicobacter/imunologia
Helicobacter pylori/imunologia
Mediadores da Inflamação/metabolismo
Estômago/patologia
[Mh] Termos MeSH secundário: Anticorpos Bloqueadores/farmacologia
Células Cultivadas
Quimiocina CXCL1/genética
Quimiocina CXCL1/metabolismo
Quimiocina CXCL5/genética
Quimiocina CXCL5/metabolismo
Células Epiteliais/microbiologia
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Seres Humanos
Interleucina-8/genética
Interleucina-8/metabolismo
Janus Quinases/metabolismo
Cultura Primária de Células
Receptor do Fator de Crescimento Epidérmico/metabolismo
Transdução de Sinais
Receptor 2 Toll-Like/imunologia
Receptor 2 Toll-Like/metabolismo
Receptor 4 Toll-Like/imunologia
Receptor 4 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Blocking); 0 (CXCL1 protein, human); 0 (CXCL5 protein, human); 0 (Chemokine CXCL1); 0 (Chemokine CXCL5); 0 (IL8 protein, human); 0 (Inflammation Mediators); 0 (Interleukin-8); 0 (TLR2 protein, human); 0 (TLR4 protein, human); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.2 (Janus Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161204
[St] Status:MEDLINE
[do] DOI:10.1177/1753425916681077


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[PMID]:27876461
[Au] Autor:Zhang D; Zhou J; Tang D; Zhou L; Chou L; Chou KY; Tao L; Lu LM
[Ad] Endereço:Department of Otolaryngology-HNS, Eye, Ear, Nose and Throat Hospital, Shanghai Key Clinical Disciplines of Otorhinolaryngology, Fudan University School of Medicine, 83 Fenyang Road, Shanghai 200031, China; Department of Pudong Hospital, Fudan University School of Medicine, 2800 Gongwei Road, Shangha
[Ti] Título:Neutrophil infiltration mediated by CXCL5 accumulation in the laryngeal squamous cell carcinoma microenvironment: A mechanism by which tumour cells escape immune surveillance.
[So] Source:Clin Immunol;175:34-40, 2017 Feb.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The CXCL5 chemokine is important for neutrophil accumulation in tumour tissues. In this report, we attempted to clarify whether and how infiltrating tumour-associated neutrophils (TANs) in laryngeal squamous cell carcinoma (LSCC) affect the proliferation and activation of T cells. We examined chemokine expression by real-time PCR (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) and performed an immunohistochemical analysis of LSCC microarrays. The relationship between CXCL5 and CD66b (a neutrophil marker) was investigated by immunofluorescence staining. We found that CXCL5 was upregulated in LSCC tissues, whereas CXCL5 levels were decreased in LSCC patient serum. Furthermore, high levels of CXCL5 were significantly correlated with intratumoural neutrophil infiltration. Compared with peripheral blood neutrophils (PBNs), TANs significantly inhibited T cell proliferation and decreased IFN-γ and TNF-α secretion. These data suggest that excessive neutrophil infiltration is associated with advanced clinical stages of LSCC (T3 or T4, III or IV, and N1 or N2).
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/imunologia
Quimiocina CXCL5/metabolismo
Neoplasias Laríngeas/imunologia
Infiltração de Neutrófilos/imunologia
Neutrófilos/imunologia
Microambiente Tumoral/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma de Células Escamosas/sangue
Carcinoma de Células Escamosas/metabolismo
Proliferação Celular/fisiologia
Quimiocina CXCL5/sangue
Feminino
Neoplasias de Cabeça e Pescoço/sangue
Neoplasias de Cabeça e Pescoço/imunologia
Neoplasias de Cabeça e Pescoço/metabolismo
Seres Humanos
Neoplasias Laríngeas/sangue
Neoplasias Laríngeas/metabolismo
Masculino
Meia-Idade
Neutrófilos/metabolismo
Linfócitos T/imunologia
Linfócitos T/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Regulação para Cima/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL5 protein, human); 0 (Chemokine CXCL5); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171008
[Lr] Data última revisão:
171008
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE


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[PMID]:27748886
[Au] Autor:Dai Z; Wu J; Chen F; Cheng Q; Zhang M; Wang Y; Guo Y; Song T
[Ad] Endereço:Institute of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.
[Ti] Título:CXCL5 promotes the proliferation and migration of glioma cells in autocrine- and paracrine-dependent manners.
[So] Source:Oncol Rep;36(6):3303-3310, 2016 Dec.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:CXCL5 and its receptor CXCR2 have been found to be involved in tumorigenesis and cancer progression. Recent studies have shown that CXCR2 is upregulated in glioma tissues, and associated with poor prognosis and recurrence. However, the role of CXCL5/CXCR2 signaling in mediating the malignant phenotypes of glioma cells, as well as the underlying mechanism, still remains unclear. In the present study, we found that CXCL5 was upregulated in glioma tissues compared to that noted in normal brain tissues. High CXCL5 levels were significantly associated with higher tumor grade, advanced clinical stage, and shorter survival time of glioma patients. In vitro studies indicated that the protein expression levels of CXCL5 and CXCR2 were markedly higher in human glioma cell lines (U87, U251, U373 and A172), when compared with those in normal human gliocyte HEB cells. Overexpression of CXLC5 significantly promoted the proliferation and migration of U87 cells, while knockdown of CXCL5 by small interfering RNA markedly inhibited U87 cell proliferation and migration. Moreover, both exogenous CXCL5 treatment and the conditioned medium of CXCL5-overexpressing HEB cells also enhanced the proliferation and migration of U87 cells. Molecular mechanism investigation revealed that CXLC5 activated the ERK, JNK, p38 MAPK signaling pathways, which play key roles in tumor growth and metastasis. According to these data, our study suggests that CXCL5 plays a promoting role in glioma in autocrine- and paracrine-dependent manners.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/metabolismo
Proliferação Celular
Quimiocina CXCL5/fisiologia
Glioma/metabolismo
[Mh] Termos MeSH secundário: Comunicação Autócrina
Neoplasias Encefálicas/patologia
Linhagem Celular Tumoral
Movimento Celular
Feminino
Glioma/patologia
Seres Humanos
Masculino
Meia-Idade
Comunicação Parácrina
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL5 protein, human); 0 (Chemokine CXCL5)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170324
[Lr] Data última revisão:
170324
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.5155



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