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[PMID]: 27338806 [Au] Autor: Rudolph H; Klopstein A; Gruber I; Blatti C; Lyck R; Engelhardt B [Ad] Endereço: Theodor Kocher Institute, University of Bern, Bern, Switzerland. [Ti] Título: Postarrest stalling rather than crawling favors CD8(+) over CD4(+) T-cell migration across the blood-brain barrier under flow in vitro. [So] Source: Eur J Immunol;46(9):2187-203, 2016 Sep. [Is] ISSN: 1521-4141 [Cp] País de publicação: Germany [La] Idioma: eng [Ab] Resumo: Although CD8(+) T cells have been implied in the pathogenesis of multiple sclerosis (MS), the molecular mechanisms mediating CD8(+) T-cell migration across the blood-brain barrier (BBB) into the central nervous system (CNS) are ill defined. Using in vitro live cell imaging, we directly compared the multistep extravasation of activated CD4(+) and CD8(+) T cells across primary mouse brain microvascular endothelial cells (pMBMECs) as a model for the BBB under physiological flow. Significantly higher numbers of CD8(+) than CD4(+) T cells arrested on pMBMECs under noninflammatory and inflammatory conditions. While CD4(+) T cells polarized and crawled prior to their diapedesis, the majority of CD8(+) T cells stalled and readily crossed the pMBMEC monolayer preferentially via a transcellular route. T-cell arrest and crawling were independent of G-protein-coupled receptor signaling. Rather, absence of endothelial ICAM-1 and ICAM-2 abolished increased arrest of CD8(+) over CD4(+) T cells and abrogated T-cell crawling, leading to the efficient reduction of CD4(+) , but to a lesser degree of CD8(+) , T-cell diapedesis across ICAM-1(null) /ICAM-2(-/-) pMBMECs. Thus, cellular and molecular mechanisms mediating the multistep extravasation of activated CD8(+) T cells across the BBB are distinguishable from those involved for CD4(+) T cells. [Mh] Termos MeSH primário: Barreira Hematoencefálica/metabolismo Linfócitos T CD4-Positivos/imunologia Linfócitos T CD4-Positivos/metabolismo Linfócitos T CD8-Positivos/imunologia Linfócitos T CD8-Positivos/metabolismo Migração Transcelular de Célula/imunologia [Mh] Termos MeSH secundário: Animais Biomarcadores Linfócitos T CD4-Positivos/efeitos dos fármacos Linfócitos T CD8-Positivos/efeitos dos fármacos Células Endoteliais/metabolismo Endotélio Vascular/metabolismo Molécula 1 de Adesão Intercelular/metabolismo Interferon gama/metabolismo Interferon gama/farmacologia Migração e Rolagem de Leucócitos/imunologia Ativação Linfocitária/imunologia Antígeno-1 Associado à Função Linfocitária/metabolismo Camundongos Camundongos Knockout Camundongos Transgênicos Fator de Necrose Tumoral alfa/metabolismo Fator de Necrose Tumoral alfa/farmacologia Molécula 1 de Adesão de Célula Vascular/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Biomarkers); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1); 126547-89-5 (Intercellular Adhesion Molecule-1); 82115-62-6 (Interferon-gamma) [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: 160625 [St] Status: MEDLINE [do] DOI: 10.1002/eji.201546251

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[PMID]: 26792186 [Au] Autor: Yang YT; Yang HY; Wang YF; Shen SY; Li MH; Qin JR [Ad] Endereço: Department of Oral and Maxillofacial Surgery, Peking University Shenzhen Hospital, Shenzhen Guangdong 518036, China. [Ti] Título: [The influence of urothelial carcinoembryonic antigen 1 on invasion and migration of oral carcinoma cell lines]. [So] Source: Zhonghua Kou Qiang Yi Xue Za Zhi;51(1):36-41, 2016 Jan. [Is] ISSN: 1002-0098 [Cp] País de publicação: China [La] Idioma: chi [Ab] Resumo: OBJECTIVE: To investigate the effects of long chain non-coding RNA urothelial carcinoembryonic antigen 1(UCA1) on invasion, migration and proliferation abilities in oral squamous cell carcinoma cell lines SCC15 and CAL27. METHODS: Small interfering RNA of UCA1(UCA1-siRNA) was transfected into SCC15 and CAL27 cell lines by Lipofectamine(TM) 3000 to silence UCA1 , and transfected negtive control si-RNA served as a control. The effect of UCA1-siRNA was detected by quantitative real time-polymerase chain reaction(qRT-PCR) to confirm the successful inhibition of UCA1 by siRNA. The matrix metalloproteinase 9(MMP-9) protein level was detected by Western blotting analysis. The effect of siRNA on cell proliferation and invasion was assessed by transwell migration assay and wound healing assay. Cell counting kit-8(CCK-8) assay was carried out to estimate the proliferation of two cell lines with different expression levels of UCA1. RESULTS: Expressions of UCA1 of SCC15 and CAL27 were successfully suppressed after transfected with siRNA which verified by qRT-PCR, and the efficiency of downregulation of SCC15 and CAL27 was 86.45%(P<0.001)and 78.24%(P<0.001), respectively. The migration, invasion and proliferation of SCC15 and CAL27 cell lines after transfected with siRNA were obviously restrained. The number of migration and invasion of CAL27 cells were 719.20±92.36 versus 208.00±25.58 (P=0.000 7) and 363.40 ± 45.96 versus 164.80 ± 24.68(P= 0.005 2), respectively, the number of migration and invasion of SCC15 cells were 437.20±54.75 vs 145.80±23.31(P=0.001 1) and 249.80±38.41 vs 63.80±11.11 (P=0.001 6), respectively (UCA1-si compare to negtive control), the relative proliferation rates of SCC15 and CAL27 were SCC15: R24 h=0.870, R48 h=0.863, R72 h=0.64, R96 h=0.732; CAL27: R24 h=0.913, R48 h=0.829, R72 h=0.756, R96 h= 0.705(P<0.05), and MMP-9 expression level was decreased by UCA1-siRNA compared with negative control. CONCLUSIONS: UCA1 could enhance the ability of invasion and migration of SCC15 and CAL27 cell lines via regulating MMP-9 protein expression, which suggests that UCA1 might play a pivotal role in oral squamous cell carcinoma invasion and progression. [Mh] Termos MeSH primário: Antígeno Carcinoembrionário/fisiologia Carcinoma de Células Escamosas/patologia Movimento Celular Proliferação Celular/fisiologia Metaloproteinase 9 da Matriz/metabolismo Neoplasias Bucais/patologia Invasividade Neoplásica RNA Interferente Pequeno Transfecção [Mh] Termos MeSH secundário: Antígeno Carcinoembrionário/genética Carcinoma de Células Escamosas/enzimologia Linhagem Celular Tumoral Inibição de Migração Celular Regulação para Baixo Seres Humanos Metaloproteinase 9 da Matriz/análise Neoplasias Bucais/enzimologia RNA Longo não Codificante Migração Transcelular de Célula [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Carcinoembryonic Antigen); 0 (RNA, Long Noncoding); 0 (RNA, Small Interfering); EC 3.4.24.35 (Matrix Metalloproteinase 9) [Em] Mês de entrada: 1707 [Cu] Atualização por classe: 170724 [Lr] Data última revisão: 170724 [Sb] Subgrupo de revista: D; IM [Da] Data de entrada para processamento: 160122 [St] Status: MEDLINE [do] DOI: 10.3760/cma.j.issn.1002-0098.2016.01.009

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[PMID]: 26744469 [Au] Autor: Halliez MC; Motta JP; Feener TD; Guérin G; LeGoff L; François A; Colasse E; Favennec L; Gargala G; Lapointe TK; Altier C; Buret AG [Ad] Endereço: Protozooses transmises par l'alimentation, Rouen University Hospital, University of Rouen and University of Reims Champagne-Ardennes, and Institute for Biomedical Research, Rouen and Reims, France; Department of Biological Sciences, Inflammation Research Network, Host-Parasite Interaction NSERC-CREA [Ti] Título: Giardia duodenalis induces paracellular bacterial translocation and causes postinfectious visceral hypersensitivity. [So] Source: Am J Physiol Gastrointest Liver Physiol;310(8):G574-85, 2016 Apr 15. [Is] ISSN: 1522-1547 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Irritable bowel syndrome (IBS) is the most frequent functional gastrointestinal disorder. It is characterized by abdominal hypersensitivity, leading to discomfort and pain, as well as altered bowel habits. While it is common for IBS to develop following the resolution of infectious gastroenteritis [then termed postinfectious IBS (PI-IBS)], the mechanisms remain incompletely understood. Giardia duodenalis is a cosmopolitan water-borne enteropathogen that causes intestinal malabsorption, diarrhea, and postinfectious complications. Cause-and-effect studies using a human enteropathogen to help investigate the mechanisms of PI-IBS are sorely lacking. In an attempt to establish causality between giardiasis and postinfectious visceral hypersensitivity, this study describes a new model of PI-IBS in neonatal rats infected with G. duodenalis At 50 days postinfection with G. duodenalis (assemblage A or B), long after the parasite was cleared, rats developed visceral hypersensitivity to luminal balloon distension in the jejunum and rectum, activation of the nociceptive signaling pathway (increased c-fos expression), histological modifications (villus atrophy and crypt hyperplasia), and proliferation of mucosal intraepithelial lymphocytes and mast cells in the jejunum, but not in the rectum. G. duodenalis infection also disrupted the intestinal barrier, in vivo and in vitro, which in turn promoted the translocation of commensal bacteria. Giardia-induced bacterial paracellular translocation in vitro correlated with degradation of the tight junction proteins occludin and claudin-4. The extensive observations associated with gut hypersensitivity described here demonstrate that, indeed, in this new model of postgiardiasis IBS, alterations to the gut mucosa and c-fos are consistent with those associated with PI-IBS and, hence, offer avenues for new mechanistic research in the field. [Mh] Termos MeSH primário: Microbioma Gastrointestinal Giardíase/complicações Síndrome do Intestino Irritável/etiologia Migração Transcelular de Célula [Mh] Termos MeSH secundário: Animais Células CACO-2 Escherichia coli/patogenicidade Escherichia coli/fisiologia Feminino Giardíase/microbiologia Seres Humanos Mucosa Intestinal/metabolismo Mucosa Intestinal/patologia Síndrome do Intestino Irritável/microbiologia Síndrome do Intestino Irritável/parasitologia Masculino Nociceptividade Ratos Ratos Sprague-Dawley Proteínas de Junções Íntimas/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Tight Junction Proteins) [Em] Mês de entrada: 1706 [Cu] Atualização por classe: 170605 [Lr] Data última revisão: 170605 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160109 [St] Status: MEDLINE [do] DOI: 10.1152/ajpgi.00144.2015

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[PMID]: 25317631 [Au] Autor: Ebrahim NA; Leach L [Ad] Endereço: Cardiovascular Research Group, School of Life Sciences, Faculty of Medicine & Health Sciences, University of Nottingham , Nottingham, United Kingdom . [Ti] Título: Temporal studies into attachment, VE-cadherin perturbation, and paracellular migration of human umbilical mesenchymal stem cells across umbilical vein endothelial monolayers. [So] Source: Stem Cells Dev;24(4):426-36, 2015 Feb 15. [Is] ISSN: 1557-8534 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Mesenchymal stem cells from Wharton's jelly of human umbilical cords (WJ-MSC) are a valuable alternate source of stem cells. Their role in situ and whether they can interact and cross intact endothelial monolayers requires elucidation. The aim of this study was to investigate the dynamic interactions between WJ-MSC and human umbilical vein endothelial cells (HUVEC), including attachment, transit times, extravasation pathway, and the effects of WJ-MSC on junctional vascular endothelial (VE)-cadherin. HUVEC were grown to near confluence in endothelial media and to full confluence in mixed media before the addition of PKH26-labelled WJ-MSC. Time lapse fluorescence microscopy showed stem cells undergoing membrane blebbing followed by amoeboid movement on HUVEC monolayers before rounding up and changing shape toward the spindle-shaped morphology during/after transmigration to subendothelial positions. Cells demonstrated a time lag of 60 min before paracellular extravasation, confirmed by confocal microscopy. Forty-six percent of attached cells crossed in the first 2 h. By 16 h, a majority of cells had transmigrated with >96% of cells crossing by 22 h. There were concomitant changes in endothelial junctional VE-cadherin with statistically significant increases in discontinuous staining at 2 h, return to control values at 16 h, even as from 22 h onward HUVEC displayed increased percentage of junctions with continuous staining and upregulation of protein. Our data suggests that WJ-MSC crosses the endothelial barrier through the paracellular pathway and can influence junctional organization of HUVEC with discreet perturbation of VE-cadherin preceding transmigration followed by upregulation once the adluminal side is reached. The latter may reflect a perivascular support function of WJ-MSC in the umbilical cord. [Mh] Termos MeSH primário: Antígenos CD/metabolismo Caderinas/metabolismo Células Endoteliais da Veia Umbilical Humana/fisiologia Células Mesenquimais Estromais/fisiologia Migração Transcelular de Célula [Mh] Termos MeSH secundário: Adesão Celular Membrana Celular/metabolismo Células Endoteliais da Veia Umbilical Humana/metabolismo Seres Humanos Células Mesenquimais Estromais/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antigens, CD); 0 (Cadherins); 0 (cadherin 5) [Em] Mês de entrada: 1510 [Cu] Atualização por classe: 161019 [Lr] Data última revisão: 161019 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 141016 [St] Status: MEDLINE [do] DOI: 10.1089/scd.2014.0207

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[PMID]: 25176655 [Au] Autor: Leong HS; Robertson AE; Stoletov K; Leith SJ; Chin CA; Chien AE; Hague MN; Ablack A; Carmine-Simmen K; McPherson VA; Postenka CO; Turley EA; Courtneidge SA; Chambers AF; Lewis JD [Ad] Endereço: Translational Prostate Cancer Research Group, London Regional Cancer Program, 790 Commissioners Road East, London ON N6A 4L6, Canada. [Ti] Título: Invadopodia are required for cancer cell extravasation and are a therapeutic target for metastasis. [So] Source: Cell Rep;8(5):1558-70, 2014 Sep 11. [Is] ISSN: 2211-1247 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Tumor cell extravasation is a key step during cancer metastasis, yet the precise mechanisms that regulate this dynamic process are unclear. We utilized a high-resolution time-lapse intravital imaging approach to visualize the dynamics of cancer cell extravasation in vivo. During intravascular migration, cancer cells form protrusive structures identified as invadopodia by their enrichment of MT1-MMP, cortactin, Tks4, and importantly Tks5, which localizes exclusively to invadopodia. Cancer cells extend invadopodia through the endothelium into the extravascular stroma prior to their extravasation at endothelial junctions. Genetic or pharmacological inhibition of invadopodia initiation (cortactin), maturation (Tks5), or function (Tks4) resulted in an abrogation of cancer cell extravasation and metastatic colony formation in an experimental mouse lung metastasis model. This provides direct evidence of a functional role for invadopodia during cancer cell extravasation and distant metastasis and reveals an opportunity for therapeutic intervention in this clinically important process. [Mh] Termos MeSH primário: Extensões da Superfície Celular/metabolismo Neoplasias Pulmonares/metabolismo Células-Tronco Neoplásicas/metabolismo Migração Transcelular de Célula [Mh] Termos MeSH secundário: Animais Antineoplásicos/farmacologia Benzodioxóis/farmacologia Linhagem Celular Tumoral Extensões da Superfície Celular/efeitos dos fármacos Embrião de Galinha Cortactina/genética Cortactina/metabolismo Feminino Seres Humanos Neoplasias Pulmonares/patologia Metaloproteinase 14 da Matriz/metabolismo Camundongos Camundongos Nus Metástase Neoplásica Células-Tronco Neoplásicas/fisiologia Fosfoproteínas/antagonistas & inibidores Fosfoproteínas/genética Fosfoproteínas/metabolismo Inibidores de Proteínas Quinases/farmacologia Quinazolinas/farmacologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Benzodioxoles); 0 (Cortactin); 0 (Fish protein, mouse); 0 (Phosphoproteins); 0 (Protein Kinase Inhibitors); 0 (Quinazolines); 0 (Tks4 protein, mouse); 9KD24QGH76 (saracatinib); EC 3.4.24.80 (Matrix Metalloproteinase 14) [Em] Mês de entrada: 1505 [Cu] Atualização por classe: 140913 [Lr] Data última revisão: 140913 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140902 [St] Status: MEDLINE

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[PMID]: 24638889 [Au] Autor: Vestweber D; Wessel F; Nottebaum AF [Ad] Endereço: Max-Planck-Institute for Molecular Biomedicine, Röntgenstr. 20, D-48149, Münster, Germany, vestweb@mpi-muenster.mpg.de. [Ti] Título: Similarities and differences in the regulation of leukocyte extravasation and vascular permeability. [So] Source: Semin Immunopathol;36(2):177-92, 2014 Mar. [Is] ISSN: 1863-2300 [Cp] País de publicação: Germany [La] Idioma: eng [Ab] Resumo: Leukocyte extravasation is regulated and mediated by a multitude of adhesion and signaling molecules. Many of them enable the capturing and docking of leukocytes to the vessel wall. Others allow leukocytes to crawl on the apical surface of endothelial cells to appropriate sites of exit. While these steps are well understood and the adhesion molecules mediating these interactions are largely identified, a still growing number of adhesion receptors mediate the diapedesis process, the actual migration of leukocytes through the endothelial cell layer, and the underlying basement membrane. In most cases, it is not known which molecular processes they actually mediate, whether they enable the migration of leukocytes through the endothelial cell layer or whether they are involved in the destabilization of endothelial junctions. In addition, leukocytes are able to circumvent junctions and transcytose directly through the body of endothelial cells. While this latter route indeed exists, recent work has highlighted in vivo the junctional pathway as the prevalent way of leukocyte exit in various inflamed tissues. Recent work elucidating molecular mechanisms that regulate endothelial junctions and thereby leukocyte extravasation and vascular permeability will be discussed. [Mh] Termos MeSH primário: Permeabilidade Capilar Leucócitos/fisiologia [Mh] Termos MeSH secundário: Actomiosina/metabolismo Animais Antígenos CD/química Antígenos CD/metabolismo Caderinas/química Caderinas/metabolismo Cateninas/metabolismo Moléculas de Adesão Celular/metabolismo Comunicação Celular Movimento Celular Citoesqueleto/metabolismo Células Endoteliais/metabolismo Endotélio Vascular/metabolismo Seres Humanos Junções Intercelulares/metabolismo Fosforilação Domínios e Motivos de Interação entre Proteínas Proteínas Tirosina Fosfatases/metabolismo Receptores de Superfície Celular/metabolismo Migração Transcelular de Célula [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Nm] Nome de substância: 0 (Antigens, CD); 0 (Cadherins); 0 (Catenins); 0 (Cell Adhesion Molecules); 0 (Receptors, Cell Surface); 0 (cadherin 5); 9013-26-7 (Actomyosin); EC 3.1.3.48 (Protein Tyrosine Phosphatases) [Em] Mês de entrada: 1412 [Cu] Atualização por classe: 170926 [Lr] Data última revisão: 170926 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140319 [St] Status: MEDLINE [do] DOI: 10.1007/s00281-014-0419-7

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[PMID]: 24587014 [Au] Autor: Arvanitis C; Khuon S; Spann R; Ridge KM; Chew TL [Ad] Endereço: Department of Cell and Molecular Biology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America. [Ti] Título: Structure and biomechanics of the endothelial transcellular circumferential invasion array in tumor invasion. [So] Source: PLoS One;9(2):e89758, 2014. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Cancer cells breach the endothelium not only through cell-cell junctions but also via individual endothelial cells (ECs), or transcellular invasion. The underlying EC forms a circular structure around the transcellular invasion pore that is dependent on myosin light chain kinase (MLCK) and myosin II regulatory light chain (RLC) phosphorylation. Here we offer mechanistic insights into transcellular invasive array formation amid persistent tensile force from activated EC myosin. Fluorescence recovery after photobleaching (FRAP) experiments, sarcomeric distance measurements using super-resolution microscopy and electron microscopy provide details about the nature of the myosin II invasion array. To probe the relationship between biomechanical forces and the tension required to maintain the curvature of contractile filaments, we targeted individual actin-myosin fibers at the invasion site for photoablation. We showed that adjacent filaments rapidly replace the ablat11ed structures. We propose that the transcellular circumferential invasion array (TCIA) provides the necessary constraint within the EC to blunt the radial compression from the invading cancer cell. [Mh] Termos MeSH primário: Células Endoteliais/fisiologia Invasividade Neoplásica/fisiopatologia Migração Transcelular de Célula/fisiologia [Mh] Termos MeSH secundário: Actomiosina/metabolismo Análise de Variância Fenômenos Biomecânicos Células Endoteliais/ultraestrutura Recuperação de Fluorescência Após Fotodegradação Células Endoteliais da Veia Umbilical Humana Seres Humanos Terapia a Laser Microscopia de Fluorescência Cadeias Leves de Miosina/metabolismo Quinase de Cadeia Leve de Miosina/metabolismo Fosforilação Resistência à Tração [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S. [Nm] Nome de substância: 0 (Myosin Light Chains); 9013-26-7 (Actomyosin); EC 2.7.11.18 (Myosin-Light-Chain Kinase) [Em] Mês de entrada: 1501 [Cu] Atualização por classe: 170601 [Lr] Data última revisão: 170601 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140304 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0089758

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[PMID]: 24440560 [Au] Autor: Barreau F; Hugot JP [Ad] Endereço: Université Paris-Diderot Sorbonne Paris-Cité, UMR 843, F-75018 Paris, France; INSERM, UMR 843, F-75018 Paris, France; Labex inflamex, F-75018 Paris, France; INSERM, UMR 1043, Centre de Physiopathologie de Toulouse, Université de Toulouse, France. Electronic address: frederick.barreau@inserm.fr. [Ti] Título: Intestinal barrier dysfunction triggered by invasive bacteria. [So] Source: Curr Opin Microbiol;17:91-8, 2014 Feb. [Is] ISSN: 1879-0364 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: The ability to control uptake across the mucosa and to protect the gut from harmful substances present in the lumen is defined as intestinal barrier function. Two routes are usually distinguished for transepithelial transport. The paracellular route allows the passage of ions and small molecules and is mainly regulated by tight junctions (TJ). The transcellular route concerns large molecules or small particles (including bacteria) and is mediated by cell endocytosis and intracellular vesicular traffic. Enteropathogenic bacteria increase the transcellular permeability, especially in the follicle-associated epithelium. They also modulate TJ opening via the redistribution of TJ proteins and the activation of the myosin light chain kinase (MLCK). This review focuses on the molecular mechanisms involved in the bacteria-induced barrier defect and briefly discusses their consequences in human diseases. [Mh] Termos MeSH primário: Bactérias Interações Hospedeiro-Patógeno Mucosa Intestinal Migração Transcelular de Célula [Mh] Termos MeSH secundário: Animais Bactérias/metabolismo Bactérias/patogenicidade Permeabilidade da Membrana Celular Seres Humanos Mucosa Intestinal/microbiologia Mucosa Intestinal/fisiopatologia Camundongos Nódulos Linfáticos Agregados [Pt] Tipo de publicação: JOURNAL ARTICLE; REVIEW [Em] Mês de entrada: 1410 [Cu] Atualização por classe: 140303 [Lr] Data última revisão: 140303 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 140121 [St] Status: MEDLINE

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[PMID]: 24277076 [Au] Autor: Hoellenriegel J; Zboralski D; Maasch C; Rosin NY; Wierda WG; Keating MJ; Kruschinski A; Burger JA [Ad] Endereço: Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX; and. [Ti] Título: The Spiegelmer NOX-A12, a novel CXCL12 inhibitor, interferes with chronic lymphocytic leukemia cell motility and causes chemosensitization. [So] Source: Blood;123(7):1032-9, 2014 Feb 13. [Is] ISSN: 1528-0020 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The CXC chemokine ligand (CXCL12, or stromal cell-derived factor-1 as previously known) plays a critical role for homing and retention of chronic lymphocytic leukemia (CLL) cells in tissues such as the bone marrow (BM). In tissues, stromal cells constitutively secrete and present CXCL12 via cell-surface-bound glycosaminoglycans (GAGs), thereby attracting CLL cells and protecting them from cytotoxic drugs, a mechanism that may account for residual disease after conventional CLL therapy. NOX-A12, an RNA oligonucleotide in L-configuration (Spiegelmer) that binds and neutralizes CXCL12, was developed for interference with CXCL12 in the tumor microenvironment and for cell mobilization. Here, we examined effects of NOX-A12 on CLL cell migration and drug sensitivity. We found that NOX-A12 effectively inhibited CXCL12-induced chemotaxis of CLL cells. In contrast, NOX-A12 increased CLL migration underneath a confluent layer of BM stromal cells (BMSCs) due to interference with the CXCL12 gradient established by BMSCs. In particular, NOX-A12 competes with GAGs such as heparin for CXCL12 binding, leading to the release of CXCL12 from stromal cell-surface-bound GAGs, and thereby to neutralization of the chemokine. Furthermore, NOX-A12 sensitizes CLL cells toward bendamustine and fludarabine in BMSC cocultures. These data demonstrate that NOX-A12 effectively interferes with CLL cell migration and BMSC-mediated drug resistance, and establishes a rationale for clinical development of NOX-A12 in combination with conventional agents in CLL. [Mh] Termos MeSH primário: Antineoplásicos/farmacologia Aptâmeros de Nucleotídeos/farmacologia Movimento Celular/efeitos dos fármacos Quimiocina CXCL12/antagonistas & inibidores Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos Leucemia Linfocítica Crônica de Células B/patologia [Mh] Termos MeSH secundário: Células Cultivadas Quimiocina CXCL12/farmacologia Avaliação Pré-Clínica de Medicamentos Sinergismo Farmacológico Seres Humanos Células Jurkat Linfócitos/efeitos dos fármacos Linfócitos/fisiologia Células Mesenquimais Estromais/efeitos dos fármacos Células Mesenquimais Estromais/fisiologia Proteínas Recombinantes/farmacologia Migração Transcelular de Célula/efeitos dos fármacos [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Aptamers, Nucleotide); 0 (CXCL12 protein, human); 0 (Chemokine CXCL12); 0 (NOX-A12); 0 (Recombinant Proteins) [Em] Mês de entrada: 1404 [Cu] Atualização por classe: 161215 [Lr] Data última revisão: 161215 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 131127 [St] Status: MEDLINE [do] DOI: 10.1182/blood-2013-03-493924

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[PMID]: 24259506 [Au] Autor: Gorina R; Lyck R; Vestweber D; Engelhardt B [Ad] Endereço: Theodor Kocher Institute, University of Bern, Bern CH-3012, Switzerland. [Ti] Título: ß2 integrin-mediated crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed blood-brain barrier. [So] Source: J Immunol;192(1):324-37, 2014 Jan 01. [Is] ISSN: 1550-6606 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: In acute neuroinflammatory states such as meningitis, neutrophils cross the blood-brain barrier (BBB) and contribute to pathological alterations of cerebral function. The mechanisms that govern neutrophil migration across the BBB are ill defined. Using live-cell imaging, we show that LPS-stimulated BBB endothelium supports neutrophil arrest, crawling, and diapedesis under physiological flow in vitro. Investigating the interactions of neutrophils from wild-type, CD11a(-/-), CD11b(-/-), and CD18(null) mice with wild-type, junctional adhesion molecule-A(-/-), ICAM-1(null), ICAM-2(-/-), or ICAM-1(null)/ICAM-2(-/-) primary mouse brain microvascular endothelial cells, we demonstrate that neutrophil arrest, polarization, and crawling required G-protein-coupled receptor-dependent activation of ß2 integrins and binding to endothelial ICAM-1. LFA-1 was the prevailing ligand for endothelial ICAM-1 in mediating neutrophil shear resistant arrest, whereas Mac-1 was dominant over LFA-1 in mediating neutrophil polarization on the BBB in vitro. Neutrophil crawling was mediated by endothelial ICAM-1 and ICAM-2 and neutrophil LFA-1 and Mac-1. In the absence of crawling, few neutrophils maintained adhesive interactions with the BBB endothelium by remaining either stationary on endothelial junctions or displaying transient adhesive interactions characterized by a fast displacement on the endothelium along the direction of flow. Diapedesis of stationary neutrophils was unchanged by the lack of endothelial ICAM-1 and ICAM-2 and occurred exclusively via the paracellular pathway. Crawling neutrophils, although preferentially crossing the BBB through the endothelial junctions, could additionally breach the BBB via the transcellular route. Thus, ß2 integrin-mediated neutrophil crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed BBB. [Mh] Termos MeSH primário: Barreira Hematoencefálica/imunologia Barreira Hematoencefálica/metabolismo Antígenos CD18/metabolismo Moléculas de Adesão Celular/metabolismo Molécula 1 de Adesão Intercelular/metabolismo Neutrófilos/fisiologia Migração Transcelular de Célula/fisiologia [Mh] Termos MeSH secundário: Animais Antígenos CD Barreira Hematoencefálica/patologia Adesão Celular Moléculas de Adesão Celular/genética Células Endoteliais/metabolismo Endotélio Vascular/imunologia Endotélio Vascular/metabolismo Endotélio Vascular/patologia Inflamação/genética Inflamação/imunologia Inflamação/metabolismo Molécula 1 de Adesão Intercelular/genética Lipopolissacarídeos/imunologia Antígeno-1 Associado à Função Linfocitária/metabolismo Antígeno de Macrófago 1/metabolismo Camundongos Camundongos Knockout Receptores Acoplados a Proteínas-G/metabolismo Transdução de Sinais [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antigens, CD); 0 (CD18 Antigens); 0 (Cell Adhesion Molecules); 0 (ICAM-2 protein, mouse); 0 (Lipopolysaccharides); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Macrophage-1 Antigen); 0 (Receptors, G-Protein-Coupled); 126547-89-5 (Intercellular Adhesion Molecule-1) [Em] Mês de entrada: 1402 [Cu] Atualização por classe: 171116 [Lr] Data última revisão: 171116 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 131122 [St] Status: MEDLINE [do] DOI: 10.4049/jimmunol.1300858

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