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  1 / 118 MEDLINE  
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[PMID]:27834807
[Au] Autor:Gunning AP; Kavanaugh D; Thursby E; Etzold S; MacKenzie DA; Juge N
[Ad] Endereço:The Gut Health and Food Safety Institute Strategic Programme, Institute of Food Research, Norwich Research Park, Norwich NR4 7UA, UK. patrick.gunning@ifr.ac.uk.
[Ti] Título:Use of Atomic Force Microscopy to Study the Multi-Modular Interaction of Bacterial Adhesins to Mucins.
[So] Source:Int J Mol Sci;17(11), 2016 Nov 08.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The mucus layer covering the gastrointestinal (GI) epithelium is critical in selecting and maintaining homeostatic interactions with our gut bacteria. However, the molecular details of these interactions are not well understood. Here, we provide mechanistic insights into the adhesion properties of the canonical mucus-binding protein (MUB), a large multi-repeat cell-surface adhesin found in inhabiting the GI tract. We used atomic force microscopy to unravel the mechanism driving MUB-mediated adhesion to mucins. Using single-molecule force spectroscopy we showed that MUB displayed remarkable adhesive properties favouring a nanospring-like adhesion model between MUB and mucin mediated by unfolding of the multiple repeats constituting the adhesin. We obtained direct evidence for MUB self-interaction; MUB-MUB followed a similar binding pattern, confirming that MUB modular structure mediated such mechanism. This was in marked contrast with the mucin adhesion behaviour presented by Galectin-3 (Gal-3), a mammalian lectin characterised by a single carbohydrate binding domain (CRD). The binding mechanisms reported here perfectly match the particular structural organization of MUB, which maximizes interactions with the mucin glycan receptors through its long and linear multi-repeat structure, potentiating the retention of bacteria within the outer mucus layer.
[Mh] Termos MeSH primário: Adesinas Bacterianas/química
Galectina 3/química
Lactobacillus reuteri/metabolismo
Mucina-3/química
Proteínas Recombinantes/química
[Mh] Termos MeSH secundário: Adesinas Bacterianas/isolamento & purificação
Adesinas Bacterianas/metabolismo
Animais
Aderência Bacteriana
Meios de Cultivo Condicionados/química
Galectina 3/genética
Galectina 3/metabolismo
Expressão Gênica
Seres Humanos
Mucosa Intestinal/química
Lactobacillus reuteri/crescimento & desenvolvimento
Microscopia de Força Atômica
Modelos Moleculares
Mucina-3/isolamento & purificação
Mucina-3/metabolismo
Ligação Proteica
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adhesins, Bacterial); 0 (Culture Media, Conditioned); 0 (Galectin 3); 0 (Mucin-3); 0 (Recombinant Proteins)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161112
[St] Status:MEDLINE


  2 / 118 MEDLINE  
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[PMID]:27563024
[Au] Autor:Yoo KS; Choi HS; Jun DW; Lee HL; Lee OY; Yoon BC; Lee KG; Paik SS; Kim YS; Lee J
[Ad] Endereço:Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea.
[Ti] Título:MUC Expression in Gallbladder Epithelial Tissues in Cholesterol-Associated Gallbladder Disease.
[So] Source:Gut Liver;10(5):851-8, 2016 Sep 15.
[Is] ISSN:2005-1212
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Gallstone pathogenesis is linked to mucin hypersecretion and bacterial infection. Several mucin genes have been identified in gallbladder epithelial cells (GBECs). We investigated MUC expression in cholesterol-associated gallbladder disease and evaluated the relationship between mucin and bacterial infection. METHODS: The present study involved 20 patients with cholesterol stones with cholecystitis, five with cholesterol stones with cholesterolosis, six with cholesterol polyps, two with gallbladder cancer, and six controls. Canine GBECs treated with lipopolysaccharide were also studied. MUC3, MUC5AC, MUC5B, and MUC6 antibodies were used for dot/slot immunoblotting and immunohistochemical studies of the gallbladder epithelial tissues, canine GBECs, and bile. Reverse-transcription polymerase chain reaction was performed to evaluate MUC3 and MUC5B expression. RESULTS: MUC3, MUC5AC, MUC5B, and MUC6 were expressed in the normal gallbladder epithelium, and of those, MUC3 and MUC5B exhibited the highest expression levels. Greatly increased levels of MUC3 and MUC5B expression were observed in the cholesterol stone group, and slightly increased levels were observed in the cholesterol polyp group; MUC3 and MUC5B mRNA was also upregulated in those groups. Canine GBECs treated with lipopolysaccharide also showed upregulation of MUC3 and MUC5B. CONCLUSIONS: The mucin genes with the highest expression levels in gallbladder tissue in cholesterol-associated diseases were MUC3 and MUC5B. Cholesterol stones and gallbladder infections were associated with increased MUC3 and MUC5B expression.
[Mh] Termos MeSH primário: Colecistite/metabolismo
Células Epiteliais/metabolismo
Doenças da Vesícula Biliar/metabolismo
Mucinas Gástricas/metabolismo
Hipercolesterolemia/metabolismo
[Mh] Termos MeSH secundário: Animais
Estudos de Casos e Controles
Colecistite/etiologia
Cães
Vesícula Biliar/citologia
Doenças da Vesícula Biliar/etiologia
Seres Humanos
Hipercolesterolemia/complicações
Mucina-5AC/metabolismo
Mucina-3/metabolismo
Mucina-5B/metabolismo
Mucina-6/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gastric Mucins); 0 (Mucin 5AC); 0 (Mucin-3); 0 (Mucin-5B); 0 (Mucin-6)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160827
[St] Status:MEDLINE
[do] DOI:10.5009/gnl15600


  3 / 118 MEDLINE  
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[PMID]:27465957
[Au] Autor:Shang XB; Zhao Q; Zhao CY
[Ad] Endereço:Department of Infectious Disease, the Third Hospital of Hebei Medical University, Shijiazhuang 050051, China.
[Ti] Título:[Association between chronicity of HBV infection and host immunity].
[So] Source:Zhonghua Gan Zang Bing Za Zhi;24(6):474-7, 2016 Jun.
[Is] ISSN:1007-3418
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:The prognosis of hepatitis B virus (HBV) infection is determined by innate immunity, adaptive immunity, and a variety of regulatory factors in the host. Controversy still exists over the role of innate immunity in the progression of HBV infection. Adaptive immunity, especially the immune response mediated by CD8+ T cells, plays an important role in HBV clearance. However, in patients with chronic infection, such CD8+ T cells are often exhausted and associated with various regulatory factors including programmed cell death 1 and T-cell immunoglobulin mucin-3. This article elaborates on the association of chronicity of HBV infection with host immune system and various regulating factors.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Hepatite B Crônica/imunologia
Imunidade Inata
[Mh] Termos MeSH secundário: Seres Humanos
Mucina-3/imunologia
Receptor de Morte Celular Programada 1/imunologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MUC3A protein, human); 0 (Mucin-3); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170126
[Lr] Data última revisão:
170126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160729
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1007-3418.2016.06.018


  4 / 118 MEDLINE  
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[PMID]:27365309
[Au] Autor:Stremmel W; Staffer S; Gan-Schreier H; Wannhoff A; Bach M; Gauss A
[Ad] Endereço:Department of Internal Medicine IV, University Clinics of Heidelberg, Heidelberg, Germany. Electronic address: wolfgang.stremmel@med.uni-heidelberg.de.
[Ti] Título:Phosphatidylcholine passes through lateral tight junctions for paracellular transport to the apical side of the polarized intestinal tumor cell-line CaCo2.
[So] Source:Biochim Biophys Acta;1861(9 Pt A):1161-1169, 2016 09.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Phosphatidylcholine (PC) is the most abundant phospholipid in intestinal mucus, indicative of a specific transport system across the mucosal epithelium to the intestinal lumen. To elucidate this transport mechanism, we employed a transwell tissue culture system with polarized CaCo2 cells. It was shown that PC could not substantially be internalized by the cells. However, after basal application of increasing PC concentrations, an apical transport of 47.1±6.3nmolh(-1)mMPC(-1) was observed. Equilibrium distribution studies with PC applied in equal concentrations to the basal and apical compartments showed a 1.5-fold accumulation on the expense of basal PC. Disruption of tight junctions (TJ) by acetaldehyde or PPARγ inhibitors or by treatment with siRNA to TJ proteins suppressed paracellular transport by at least 50%. Transport was specific for the choline containing the phospholipids PC, lysoPC and sphingomyelin. We showed that translocation is driven by an electrochemical gradient generated by apical accumulation of Cl(-) and HCO3(-) through CFTR. Pretreatment with siRNA to mucin 3 which anchors in the apical plasma membrane of mucosal cells inhibited the final step of luminal PC secretion. PC accumulates in intestinal mucus using a paracellular, apically directed transport route across TJs.
[Mh] Termos MeSH primário: Mucosa Intestinal/metabolismo
Neoplasias Intestinais/metabolismo
Fosfatidilcolinas/metabolismo
Junções Íntimas/metabolismo
[Mh] Termos MeSH secundário: Células CACO-2
Permeabilidade da Membrana Celular/genética
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Epitélio/metabolismo
Seres Humanos
Mucosa Intestinal/patologia
Neoplasias Intestinais/patologia
Mucina-3/antagonistas & inibidores
Mucina-3/genética
PPAR gama/antagonistas & inibidores
PPAR gama/metabolismo
Fosfatidilcolinas/secreção
RNA Interferente Pequeno/genética
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CFTR protein, human); 0 (Mucin-3); 0 (PPAR gamma); 0 (Phosphatidylcholines); 0 (RNA, Small Interfering); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160702
[St] Status:MEDLINE


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[PMID]:27259857
[Au] Autor:Erickson JJ; Rogers MC; Tollefson SJ; Boyd KL; Williams JV
[Ad] Endereço:Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232;
[Ti] Título:Multiple Inhibitory Pathways Contribute to Lung CD8+ T Cell Impairment and Protect against Immunopathology during Acute Viral Respiratory Infection.
[So] Source:J Immunol;197(1):233-43, 2016 Jul 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viruses are frequent causes of lower respiratory infection (LRI). Programmed cell death-1 (PD-1) signaling contributes to pulmonary CD8(+) T cell (TCD8) functional impairment during acute viral LRI, but the role of TCD8 impairment in viral clearance and immunopathology is unclear. We now find that human metapneumovirus infection induces virus-specific lung TCD8 that fail to produce effector cytokines or degranulate late postinfection, with minimally increased function even in the absence of PD-1 signaling. Impaired lung TCD8 upregulated multiple inhibitory receptors, including PD-1, lymphocyte activation gene 3 (LAG-3), T cell Ig mucin 3, and 2B4. Moreover, coexpression of these receptors continued to increase even after viral clearance, with most virus-specific lung TCD8 expressing three or more inhibitory receptors on day 14 postinfection. Viral infection also increased expression of inhibitory ligands by both airway epithelial cells and APCs, further establishing an inhibitory environment. In vitro Ab blockade revealed that multiple inhibitory receptors contribute to TCD8 impairment induced by either human metapneumovirus or influenza virus infection. In vivo blockade of T cell Ig mucin 3 signaling failed to enhance TCD8 function or reduce viral titers. However, blockade of LAG-3 in PD-1-deficient mice restored TCD8 effector functions but increased lung pathology, indicating that LAG-3 mediates lung TCD8 impairment in vivo and contributes to protection from immunopathology during viral clearance. These results demonstrate that an orchestrated network of pathways modifies lung TCD8 functionality during viral LRI, with PD-1 and LAG-3 serving prominent roles. Lung TCD8 impairment may prevent immunopathology but also contributes to recurrent lung infections.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Vírus da Influenza A Subtipo H1N1/imunologia
Pulmão/imunologia
Metapneumovirus/imunologia
Infecções por Orthomyxoviridae/imunologia
Infecções por Paramyxoviridae/imunologia
Infecções Respiratórias/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Linfócitos T CD8-Positivos/virologia
Células Cultivadas
Pulmão/virologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Mucina-3/metabolismo
Receptor de Morte Celular Programada 1/genética
Infecções Respiratórias/virologia
Transdução de Sinais
Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD223 antigen); 0 (Cd244 protein, mouse); 0 (Mucin-3); 0 (Pdcd1 protein, mouse); 0 (Programmed Cell Death 1 Receptor); 0 (Signaling Lymphocytic Activation Molecule Family)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160605
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1502115


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[PMID]:26459727
[Au] Autor:Yang Q; Zhou Y; Li FY; Mao H; Shrestha A; Ma WJ; Cheng NS; Zhang W
[Ad] Endereço:Department of Hepatobiliary Surgery, West China Hospital of Sichuan University, Chengdu 610041, China. lfy_74@vip.163.com.
[Ti] Título:Effects of epidermal growth factor receptor inhibitor on proliferative cholangitis in hepatolithiasis.
[So] Source:Hepatobiliary Pancreat Dis Int;14(5):509-15, 2015 Oct.
[Is] ISSN:1499-3872
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: There is currently no effective medication to prevent stone recurrence after choledochoscopic lithotomy or to treat proliferative cholangitis (PC), which is the pathologic basis of hepatolithiasis. This study aimed to investigate whether gefitinib, an epidermal growth factor receptor (EGFR) inhibitor, inhibited cholangio hyperplasia and lithogenesis in PC. METHODS: After cholangioscopic lithotomy, indwelling catheters were placed in the diseased bile duct lumens in 94 patients with hepatolithiasis. Subsequently, 49 of the 94 patients were treated with 250 mg gefitinib solution via a catheter twice a week, and they were subjected to choledochoscopic biopsy at 6 and 12 weeks. The rest 45 hepatolithiasis patients without gefitinib treatment served as controls. RESULTS: The expressions of EGFR, PCNA and procollagen I were significantly reduced in the patients treated with gefitinib in 12 weeks compared with those in the control group. Patients in the gefitinib group had a much lower degree of hyperplasia of the biliary epithelium, submucosal glands and collagen fibers compared with those in the control group. Gefitinib treatment significantly decreased mucin 3 expression and beta-glucuronidase activity. CONCLUSION: Postoperative gefitinib treatment could significantly inhibit PC-mediated hyperplasia and lithogenesis, which might provide a novel strategy for the prevention of biliary restenosis and stone recurrence in patients with hepatolithiasis.
[Mh] Termos MeSH primário: Ductos Biliares/patologia
Colangite/tratamento farmacológico
Litíase/etiologia
Hepatopatias/etiologia
Inibidores de Proteínas Quinases/uso terapêutico
Quinazolinas/uso terapêutico
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adulto
Idoso
Colangite/genética
Colangite/metabolismo
Colangite/patologia
Colágeno Tipo I/genética
Endoscopia do Sistema Digestório
Epitélio/patologia
Feminino
Expressão Gênica
Glucuronidase/metabolismo
Seres Humanos
Hiperplasia/tratamento farmacológico
Antígeno Ki-67/análise
Masculino
Meia-Idade
Mucina-3/genética
Antígeno Nuclear de Célula em Proliferação/genética
Inibidores de Proteínas Quinases/administração & dosagem
Quinazolinas/administração & dosagem
Receptor do Fator de Crescimento Epidérmico/análise
Receptor do Fator de Crescimento Epidérmico/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Ki-67 Antigen); 0 (Mucin-3); 0 (Proliferating Cell Nuclear Antigen); 0 (Protein Kinase Inhibitors); 0 (Quinazolines); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 3.2.1.31 (Glucuronidase); S65743JHBS (gefitinib)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151013
[Lr] Data última revisão:
151013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151014
[St] Status:MEDLINE


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[PMID]:25974250
[Au] Autor:Gouyer V; Dubuquoy L; Robbe-Masselot C; Neut C; Singer E; Plet S; Geboes K; Desreumaux P; Gottrand F; Desseyn JL
[Ad] Endereço:1] LIRIC - UMR 995 Inserm; Université de Lille, Lille, France [2] CHRU de Lille, Lille, France.
[Ti] Título:Delivery of a mucin domain enriched in cysteine residues strengthens the intestinal mucous barrier.
[So] Source:Sci Rep;5:9577, 2015 May 14.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A weakening of the gut mucous barrier permits an increase in the access of intestinal luminal contents to the epithelial cells, which will trigger the inflammatory response. In inflammatory bowel diseases, there is an inappropriate and ongoing activation of the immune system, possibly because the intestinal mucus is less protective against the endogenous microflora. General strategies aimed at improving the protection of the intestinal epithelium are still missing. We generated a transgenic mouse that secreted a molecule consisting of 12 consecutive copies of a mucin domain into its intestinal mucus, which is believed to modify the mucus layer by establishing reversible interactions. We showed that the mucus gel was more robust and that mucin O-glycosylation was altered. Notably, the gut epithelium of transgenic mice housed a greater abundance of beneficial Lactobacillus spp. These modifications were associated with a reduced susceptibility of transgenic mice to chemically induced colitis. Furthermore, transgenic mice cleared faster Citrobacter rodentium bacteria which were orally given and mice were more protected against bacterial translocation induced by gavage with adherent-invasive Escherichia coli. Our data show that delivering the mucin CYS domain into the gut lumen strengthens the intestinal mucus blanket which is impaired in inflammatory bowel diseases.
[Mh] Termos MeSH primário: Microbioma Gastrointestinal/imunologia
Mucosa Intestinal/metabolismo
Mucina-2/metabolismo
Muco/metabolismo
Junções Íntimas/fisiologia
[Mh] Termos MeSH secundário: Animais
Citrobacter rodentium/imunologia
Cisteína/química
Células Epiteliais
Escherichia coli/imunologia
Glicosilação
Células Caliciformes
Doenças Inflamatórias Intestinais/imunologia
Doenças Inflamatórias Intestinais/metabolismo
Mucosa Intestinal/citologia
Mucosa Intestinal/microbiologia
Intestinos/microbiologia
Lactobacillus/isolamento & purificação
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microesferas
Mucina-1/metabolismo
Mucina-2/genética
Mucina-3/metabolismo
Mucina-6/metabolismo
Estrutura Terciária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Muc2 protein, mouse); 0 (Muc3 protein, mouse); 0 (Muc6 protein, mouse); 0 (Mucin-1); 0 (Mucin-2); 0 (Mucin-3); 0 (Mucin-6); 0 (muc1 protein, mouse); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:160615
[Lr] Data última revisão:
160615
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150515
[St] Status:MEDLINE
[do] DOI:10.1038/srep09577


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[PMID]:25774422
[Au] Autor:Shimizu H; Baba N; Nose T; Taguchi R; Tanaka S; Joe GH; Maseda H; Nomura N; Hagio M; Lee JY; Fukiya S; Yokota A; Ishizuka S; Miyazaki H
[Ad] Endereço:a Research Faculty of Agriculture, Division of Applied Bioscience , Hokkaido University , Sapporo , Japan.
[Ti] Título:Activity of ERK regulates mucin 3 expression and is involved in undifferentiated Caco-2 cell death induced by 3-oxo-C12-homoserine lactone.
[So] Source:Biosci Biotechnol Biochem;79(6):937-42, 2015.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The signal molecule, 3-oxo-C12-homoserine lactone (3-oxo-C12-HSL), is similar to a mammalian hormone in bacteria. Although most studies have examined the effects of high 3-oxo-C12-HSL concentrations (>200 µM) on mammalian cellular functions because ~600 µM 3-oxo-C12-HSL can be secreted in biofilms of Pseudomonas aeruginosa grown in vitro, we previously showed that a low 3-oxo-C12-HSL concentration (30 µM) induces the apoptosis of undifferentiated Caco-2 cells through suppressing Akt activity. Here, we found that a low concentration of 3-oxo-C12-HSL-activated ERK1/2 in undifferentiated Caco-2 cells. Incubating cells with the ERK pathway inhibitor U0126 for 30 min alleviated the mucin 3 (MUC3) expression suppressed by 3-oxo-C12-HSL, and the upregulation of MUC3 expression induced by a 48-h incubation with U0126-reduced cell death. Thus, altered MUC3 expression caused by long-term attenuated ERK1/2 activity might correlate with the death of undifferentiated Caco-2 cells induced by 3-oxo-C12-HSL.
[Mh] Termos MeSH primário: 4-Butirolactona/análogos & derivados
Homosserina/análogos & derivados
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Mucina-3/genética
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: 4-Butirolactona/farmacologia
Células CACO-2
Morte Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Ativação Enzimática/efeitos dos fármacos
Homosserina/farmacologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mucin-3); 0 (N-(3-oxododecanoyl)homoserine lactone); 6KA95X0IVO (Homoserine); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); OL659KIY4X (4-Butyrolactone)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150613
[Lr] Data última revisão:
150613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150317
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2015.1006570


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[PMID]:25727397
[Au] Autor:Pinton P; Graziani F; Pujol A; Nicoletti C; Paris O; Ernouf P; Di Pasquale E; Perrier J; Oswald IP; Maresca M
[Ad] Endereço:INRA, UMR1331, Toxalim, Research Centre in Food Toxicology, Toulouse, France.
[Ti] Título:Deoxynivalenol inhibits the expression by goblet cells of intestinal mucins through a PKR and MAP kinase dependent repression of the resistin-like molecule ß.
[So] Source:Mol Nutr Food Res;59(6):1076-87, 2015 Jun.
[Is] ISSN:1613-4133
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:SCOPE: The food-associated mycotoxin deoxynivalenol (DON) is known to affect intestinal functions. However, its effect on intestinal mucus is poorly characterized. METHODS AND RESULTS: We analyzed the effects of DON on human goblet cells (HT29-16E cells) and porcine intestinal explants. Results showed that subtoxic doses of DON (as low as 1 µM) decreased mucin (MUC) production. qPCR analysis demonstrated that this inhibition was due to a specific decrease in the level of mRNA encoding for the intestinal membrane-associated (MUC1) and the secreted MUCs (MUC2, MUC3). Mechanistic studies demonstrated that DON effect relied on the activation of the protein kinase R and the mitogen-activated protein kinase p38 ultimately leading to the inhibition of the expression of resistin-like molecule beta, a known positive regulator of MUC expression. CONCLUSION: Taken together, our results show that at low doses found in food and feed, DON is able to affect the expression and production of MUCs by human and animal goblet cells. Due to the important role of MUCs in the barrier function and in the interaction of commensal bacteria with the host, such effect could explain the observed modifications in the microbial diversity and the increased susceptibility to enteric infection following exposure to DON.
[Mh] Termos MeSH primário: Células Caliciformes/efeitos dos fármacos
Intestinos/efeitos dos fármacos
Tricotecenos/toxicidade
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Regulação da Expressão Gênica
Células HT29
Seres Humanos
Mucosa Intestinal/citologia
Mucosa Intestinal/efeitos dos fármacos
Mucosa Intestinal/metabolismo
Intestinos/citologia
Intestinos/metabolismo
Masculino
Mucina-1/genética
Mucina-1/metabolismo
Mucina-2/genética
Mucina-2/metabolismo
Mucina-3/genética
Mucina-3/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Resistina/genética
Resistina/metabolismo
Suínos
Proteínas Quinases p38 Ativadas por Mitógeno/genética
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MUC1 protein, human); 0 (MUC2 protein, human); 0 (MUC3A protein, human); 0 (Mucin-1); 0 (Mucin-2); 0 (Mucin-3); 0 (RNA, Messenger); 0 (Resistin); 0 (Trichothecenes); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); JT37HYP23V (deoxynivalenol)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150603
[Lr] Data última revisão:
150603
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150303
[St] Status:MEDLINE
[do] DOI:10.1002/mnfr.201500005


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[PMID]:25630032
[Au] Autor:Menchicchi B; Fuenzalida JP; Hensel A; Swamy MJ; David L; Rochas C; Goycoolea FM
[Ad] Endereço:Westfälische Wilhelms-Universität Münster , Institute of Plant Biology and Biotechnology (IBBP), Schlossgarten 3, 48149 - Münster, Germany.
[Ti] Título:Biophysical analysis of the molecular interactions between polysaccharides and mucin.
[So] Source:Biomacromolecules;16(3):924-35, 2015 Mar 09.
[Is] ISSN:1526-4602
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mucoadhesive materials adhere persistently to mucosal surfaces. A mucoadhesive delivery system could therefore facilitate the controlled release of drugs and optimize their bioavailability in mucosal tissues. Polysaccharides are the most versatile class of natural polymers for transmucosal drug delivery. We used microviscosimetry to explore the mucoadhesion of a library of polysaccharide families with diverse structural characteristics as a first step toward the rational design of mucoadhesive polysaccharide-based nanoformulations. Here we show that the magnitude of deviation between the viscosity of mixed polysaccharide-mucin solutions and the corresponding individual stock solutions can indicate underlying molecular interactions. We found that nonlinear monotonic curves predicted a correlation between the magnitude of interaction and the ability of polysaccharide coils to contract in the presence of salt (i.e., chain flexibility). Charge-neutral polysaccharides such as dextran and Streptococcus thermophilus exopolysaccharide did not interact with mucin. Synchrotron small-angle X-ray scattering (SAXS) data supported the previously described structural features of mucin. Furthermore, high-q scattering data (i.e., sensitive to smaller scales) revealed that when mucin is in dilute solution (presumably in an extended conformation) in the presence of low-Mw alginate, its structure resembles that observed at higher concentrations in the absence of alginate. This effect was less pronounced in the case of high-Mw alginate, but the latter influenced the bulk properties of mucin-alginate mixtures (e.g., hydrodynamic radius and relative viscosity) more prominently than its low-Mw counterpart.
[Mh] Termos MeSH primário: Mucina-3/química
Polissacarídeos/química
[Mh] Termos MeSH secundário: Animais
Sistemas de Liberação de Medicamentos
Peso Molecular
Tamanho da Partícula
Ligação Proteica
Espalhamento a Baixo Ângulo
Sus scrofa
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mucin-3); 0 (Polysaccharides)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150309
[Lr] Data última revisão:
150309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150129
[St] Status:MEDLINE
[do] DOI:10.1021/bm501832y



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