Base de dados : MEDLINE
Pesquisa : G04.198.950 [Categoria DeCS]
Referências encontradas : 590 [refinar]
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[PMID]:28467903
[Au] Autor:Vaahtomeri K; Brown M; Hauschild R; De Vries I; Leithner AF; Mehling M; Kaufmann WA; Sixt M
[Ad] Endereço:Institute of Science and Technology Austria (IST Austria), Am Campus 1, 3400 Klosterneuburg, Austria; Wihuri Research Institute and Translational Cancer Biology Program, Research Program Unit, University of Helsinki, Biomedicum Helsinki, Haartmaninkatu 8, 00290 Helsinki, Finland. Electronic address:
[Ti] Título:Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.
[So] Source:Cell Rep;19(5):902-909, 2017 May 02.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration.
[Mh] Termos MeSH primário: Quimiocina CCL21/metabolismo
Células Dendríticas/fisiologia
Células Endoteliais/fisiologia
Endotélio Linfático/citologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio
Quimiocina CCL21/secreção
Células Dendríticas/metabolismo
Células Endoteliais/metabolismo
Endotélio Linfático/fisiologia
Feminino
Junções Intercelulares/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL21)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:28928095
[Au] Autor:English WR; Siviter RJ; Hansen M; Murphy G
[Ad] Endereço:University of Cambridge Department of Oncology, Cancer Research UK Cambridge Institute, Li Ka Shing Centre, Robinson Way, Cambridge, CB2 0RE, UK; Tumour Microcirculation Group, Department of Oncology and Metabolism, The Medical School, University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK.
[Ti] Título:ADAM9 is present at endothelial cell - cell junctions and regulates monocyte - endothelial transmigration.
[So] Source:Biochem Biophys Res Commun;493(2):1057-1062, 2017 Nov 18.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have found that A Disintegrin And Metalloproteinase-9 (ADAM9) localises to cell-cell junctions with VE-Cadherin in confluent endothelial monolayers. Co-cultures of cells separately transfected with ADAM9-EGFP or ADAM9-HA showed expression is required in two adjacent cells for localisation to cell-cell junctions suggesting the ADAM9 ectodomain may self-associate. A direct interaction between ADAM9 ectodomains was confirmed using recombinant proteins and an ELISA based method. As the ADAM9 ectodomain can also exist as a soluble form physiologically, we examined if this could inhibit endothelial functions dependent on cell-cell junctions. The soluble ADAM9 ectodomain could not increase endothelial monolayer permeability or inhibit monocyte-endothelial adhesion, but could inhibit monocyte-endothelial transmigration. These novel findings point to ADAM9 playing an important role in endothelial cell biology that is distinct from the other ADAMs.
[Mh] Termos MeSH primário: Proteínas ADAM/metabolismo
Células Endoteliais/citologia
Junções Intercelulares/metabolismo
Proteínas de Membrana/metabolismo
Monócitos/citologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Proteínas ADAM/análise
Animais
Linhagem Celular
Células Endoteliais/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Junções Intercelulares/ultraestrutura
Proteínas de Membrana/análise
Camundongos
Monócitos/metabolismo
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAM9 protein, human); EC 3.4.24.- (Adam9 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


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[PMID]:28916665
[Au] Autor:Cui LL; Nitzsche F; Pryazhnikov E; Tibeykina M; Tolppanen L; Rytkönen J; Huhtala T; Mu JW; Khiroug L; Boltze J; Jolkkonen J
[Ad] Endereço:From the Institute of Clinical Medicine-Neurology, University of Eastern Finland, Kuopio, Finland (L.-l.C., J.-w.M., J.J.); Department of Cell Therapy, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany (F.N.); McGowan Institute for Regenerative Medicine, University of Pittsburgh
[Ti] Título:Integrin α4 Overexpression on Rat Mesenchymal Stem Cells Enhances Transmigration and Reduces Cerebral Embolism After Intracarotid Injection.
[So] Source:Stroke;48(10):2895-2900, 2017 Oct.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Very late antigen-4 (integrin α4ß1)/vascular cell adhesion molecule-1 mediates leukocyte trafficking and transendothelial migration after stroke. Mesenchymal stem cells (MSCs) typically express integrin ß1 but insufficient ITGA4 (integrin α4), which limits their homing after intravascular transplantation. We tested whether ITGA4 overexpression on MSCs increases cerebral homing after intracarotid transplantation and reduces MSC-borne cerebral embolism. METHODS: Rat MSCs were lentivirally transduced to overexpress ITGA4. In vitro transendothelial migration was assessed using a Boyden chamber assay. Male Wistar rats intracarotidly received 0.5×10 control or modified MSCs 24 hours after sham or stroke surgery. In vivo behavior of MSCs in the cerebral vasculature was observed by intravital microscopy and single-photon emission computed tomography for up to 72 hours. RESULTS: Transendothelial migration of ITGA4-overexpressing MSCs was increased in vitro. MSCs were passively entrapped in microvessels in vivo and occasionally formed large cell aggregates causing local blood flow interruptions. MSCs were rarely found in perivascular niches or parenchyma at 72 hours post-transplantation, but ITGA4 overexpression significantly decreased cell aggregation and ameliorated the evoked cerebral embolism in stroke rats. CONCLUSIONS: ITGA4 overexpression on MSCs enhances transendothelial migration in vitro, but not in vivo, although it improves safety after intracarotid transplantation into stroke rats.
[Mh] Termos MeSH primário: Integrina alfa4/administração & dosagem
Integrina alfa4/biossíntese
Embolia Intracraniana/terapia
Células Mesenquimais Estromais/metabolismo
Transplante de Células-Tronco/métodos
Migração Transendotelial e Transepitelial/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Expressão Gênica
Injeções Intra-Arteriais
Integrina alfa4/genética
Embolia Intracraniana/diagnóstico por imagem
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
143198-26-9 (Integrin alpha4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.117.017809


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[PMID]:28893958
[Au] Autor:Zheng L; Kelly CJ; Battista KD; Schaefer R; Lanis JM; Alexeev EE; Wang RX; Onyiah JC; Kominsky DJ; Colgan SP
[Ad] Endereço:Mucosal Inflammation Program, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045.
[Ti] Título:Microbial-Derived Butyrate Promotes Epithelial Barrier Function through IL-10 Receptor-Dependent Repression of Claudin-2.
[So] Source:J Immunol;199(8):2976-2984, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Commensal interactions between the enteric microbiota and distal intestine play important roles in regulating human health. Short-chain fatty acids (SCFAs), such as butyrate, produced through anaerobic microbial metabolism represent a major energy source for the host colonic epithelium and enhance epithelial barrier function through unclear mechanisms. Separate studies revealed that the epithelial anti-inflammatory IL-10 receptor α subunit (IL-10RA) is also important for barrier formation. Based on these findings, we examined if SCFAs promote epithelial barrier through IL-10RA-dependent mechanisms. Using human intestinal epithelial cells (IECs), we discovered that SCFAs, particularly butyrate, enhanced IEC barrier formation, induced IL-10RA mRNA, IL-10RA protein, and transactivation through activated Stat3 and HDAC inhibition. Loss and gain of IL-10RA expression directly correlates with IEC barrier formation and butyrate represses permeability-promoting claudin-2 tight-junction protein expression through an IL-10RA-dependent mechanism. Our findings provide a novel mechanism by which microbial-derived butyrate promotes barrier through IL-10RA-dependent repression of claudin-2.
[Mh] Termos MeSH primário: Bactérias Anaeróbias/fisiologia
Butiratos/metabolismo
Colo/patologia
Microbioma Gastrointestinal/imunologia
Mucosa Intestinal/fisiologia
Receptores de Interleucina-10/metabolismo
Junções Íntimas/metabolismo
[Mh] Termos MeSH secundário: Butiratos/imunologia
Linhagem Celular
Células Cultivadas
Claudina-2/metabolismo
Regulação da Expressão Gênica
Histona Desacetilases/metabolismo
Seres Humanos
Mucosa Intestinal/microbiologia
Mucosa Intestinal/patologia
Receptores de Interleucina-10/genética
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Simbiose
Ativação Transcricional
Migração Transendotelial e Transepitelial
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Claudin-2); 0 (Receptors, Interleukin-10); 0 (STAT3 Transcription Factor); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700105


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[PMID]:28887431
[Au] Autor:Yonker LM; Pazos MA; Lanter BB; Mou H; Chu KK; Eaton AD; Bonventre JV; Tearney GJ; Rajagopal J; Hurley BP
[Ad] Endereço:Mucosal Immunology and Biology Research Center, Massachusetts General Hospital, Boston, MA 02114.
[Ti] Título:Neutrophil-Derived Cytosolic PLA2α Contributes to Bacterial-Induced Neutrophil Transepithelial Migration.
[So] Source:J Immunol;199(8):2873-2884, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Eicosanoids are a group of bioactive lipids that are shown to be important mediators of neutrophilic inflammation; selective targeting of their function confers therapeutic benefit in a number of diseases. Neutrophilic airway diseases, including cystic fibrosis, are characterized by excessive neutrophil infiltration into the airspace. Understanding the role of eicosanoids in this process may reveal novel therapeutic targets. The eicosanoid hepoxilin A3 is a pathogen-elicited epithelial-produced neutrophil chemoattractant that directs transepithelial migration in response to infection. Following hepoxilin A3-driven transepithelial migration, neutrophil chemotaxis is amplified through neutrophil production of a second eicosanoid, leukotriene B4 (LTB4). The rate-limiting step of eicosanoid generation is the liberation of arachidonic acid by phospholipase A2, and the cytosolic phospholipase A2 (cPLA2)α isoform has been specifically shown to direct LTB4 synthesis in certain contexts. Whether cPLA2α is directly responsible for neutrophil synthesis of LTB4 in the context of induced neutrophil transepithelial migration has not been explored. Human and mouse neutrophil epithelial cocultures were used to evaluate the role of neutrophil-derived cPLA2α in infection-induced transepithelial signaling by pharmacological and genetic approaches. Primary human airway basal stem cell derived epithelial cultures and micro-optical coherence tomography, a new imaging modality that captures two- and three-dimensional real-time dynamics of neutrophil transepithelial migration, were applied. Evidence from these studies suggests that cPLA2α expressed by neutrophils, but not epithelial cells, plays a significant role in infection-induced neutrophil transepithelial migration by mediating LTB4 synthesis during migration, which serves to amplify the magnitude of neutrophil recruitment in response to epithelial infection.
[Mh] Termos MeSH primário: Antígenos de Plaquetas Humanas/metabolismo
Fibrose Cística/imunologia
Neutrófilos/imunologia
Infecções por Pseudomonas/imunologia
Pseudomonas aeruginosa/imunologia
Mucosa Respiratória/imunologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Ácido 8,11,14-Eicosatrienoico/análogos & derivados
Ácido 8,11,14-Eicosatrienoico/metabolismo
Animais
Comunicação Celular
Linhagem Celular
Quimiotaxia
Técnicas de Cocultura
Citosol/metabolismo
Seres Humanos
Leucotrieno B4/metabolismo
Camundongos
Neutrófilos/microbiologia
Mucosa Respiratória/microbiologia
Mucosa Respiratória/patologia
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Human Platelet); 0 (human platelet antigen 1b); 1HGW4DR56D (Leukotriene B4); 7324-41-6 (8,11,14-Eicosatrienoic Acid); 85589-24-8 (8-hydroxy-11,12-epoxyeicosa-5,9,14-trienoic acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700539


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[PMID]:28808157
[Au] Autor:Bhowmick R; Clark S; Bonventre JV; Leong JM; McCormick BA
[Ad] Endereço:School of Chemical Engineering, Oklahoma State University, Stillwater, Oklahoma, USA.
[Ti] Título:Cytosolic Phospholipase A α Promotes Pulmonary Inflammation and Systemic Disease during Streptococcus pneumoniae Infection.
[So] Source:Infect Immun;85(11), 2017 Nov.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pulmonary infection by is characterized by a robust alveolar infiltration of neutrophils (polymorphonuclear cells [PMNs]) that can promote systemic spread of the infection if not resolved. We previously showed that 12-lipoxygenase (12-LOX), which is required to generate the PMN chemoattractant hepoxilin A (HXA ) from arachidonic acid (AA), promotes acute pulmonary inflammation and systemic infection after lung challenge with As phospholipase A (PLA ) promotes the release of AA, we investigated the role of PLA in local and systemic disease during infection. The group IVA cytosolic isoform of PLA (cPLA α) was activated upon infection of cultured lung epithelial cells and was critical for AA release from membrane phospholipids. Pharmacological inhibition of this enzyme blocked -induced PMN transepithelial migration Genetic ablation of the cPLA isoform cPLA α dramatically reduced lung inflammation in mice upon high-dose pulmonary challenge with The cPLA α-deficient mice also suffered no bacteremia and survived a pulmonary challenge that was lethal to wild-type mice. Our data suggest that cPLA α plays a crucial role in eliciting pulmonary inflammation during pneumococcal infection and is required for lethal systemic infection following lung challenge.
[Mh] Termos MeSH primário: Células Epiteliais/imunologia
Fosfolipases A2 do Grupo IV/imunologia
Interações Hospedeiro-Patógeno
Pulmão/imunologia
Infecções Pneumocócicas/imunologia
Pneumonia Bacteriana/imunologia
[Mh] Termos MeSH secundário: Animais
Ácido Araquidônico/imunologia
Ácido Araquidônico/metabolismo
Bacteriemia/genética
Bacteriemia/imunologia
Bacteriemia/prevenção & controle
Linhagem Celular Tumoral
Fatores Quimiotáticos/imunologia
Fatores Quimiotáticos/metabolismo
Clorobenzoatos/farmacologia
Cinamatos/farmacologia
Cicloexanonas/farmacologia
Inibidores Enzimáticos/farmacologia
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/enzimologia
Células Epiteliais/microbiologia
Fosfolipases A2 do Grupo IV/antagonistas & inibidores
Fosfolipases A2 do Grupo IV/deficiência
Fosfolipases A2 do Grupo IV/genética
Seres Humanos
Pulmão/efeitos dos fármacos
Pulmão/enzimologia
Pulmão/microbiologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Infiltração de Neutrófilos/efeitos dos fármacos
Neutrófilos/efeitos dos fármacos
Neutrófilos/imunologia
Neutrófilos/microbiologia
Infecções Pneumocócicas/genética
Infecções Pneumocócicas/microbiologia
Infecções Pneumocócicas/mortalidade
Pneumonia Bacteriana/genética
Pneumonia Bacteriana/microbiologia
Pneumonia Bacteriana/mortalidade
Streptococcus pneumoniae/efeitos dos fármacos
Streptococcus pneumoniae/genética
Streptococcus pneumoniae/patogenicidade
Análise de Sobrevida
Migração Transendotelial e Transepitelial/efeitos dos fármacos
Migração Transendotelial e Transepitelial/imunologia
ortoaminobenzoatos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemotactic Factors); 0 (Chlorobenzoates); 0 (Cinnamates); 0 (Cyclohexanones); 0 (Enzyme Inhibitors); 0 (ortho-Aminobenzoates); 110683-10-8 (4-amylcinnamoylanthranilic acid); 27YG812J1I (Arachidonic Acid); 83654-05-1 (1,6-bis(cyclohexyloximinocarbonyl)hexane); 99754-06-0 (2-(4-amylcinnamoyl)amino-4-chlorobenzoic acid); EC 3.1.1.4 (Group IV Phospholipases A2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


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[PMID]:28790198
[Au] Autor:Mittal M; Nepal S; Tsukasaki Y; Hecquet CM; Soni D; Rehman J; Tiruppathi C; Malik AB
[Ad] Endereço:From the Department of Pharmacology (M.M., S.N., Y.T., C.M.H., D.S., J.L., C.T., A.B.M.), and Department of Medicine, University of Illinois College of Medicine (J.L.).
[Ti] Título:Neutrophil Activation of Endothelial Cell-Expressed TRPM2 Mediates Transendothelial Neutrophil Migration and Vascular Injury.
[So] Source:Circ Res;121(9):1081-1091, 2017 Oct 13.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: TRPM2 (transient receptor potential melastatin-2) expressed in endothelial cells (ECs) is a cation channel mediating Ca entry in response to intracellular generation of adenosine diphosphoribose-the TRPM2 ligand. OBJECTIVE: Because polymorphonuclear neutrophils (PMN) interaction with ECs generates reactive oxygen species, we addressed the possible role of TRPM2 expressed in ECs in the mechanism of transendothelial migration of PMNs. METHODS AND RESULTS: We observed defective PMN transmigration in response to lipopolysaccharide challenge in adult mice in which the EC expressed TRPM2 is conditionally deleted ( ). PMN interaction with ECs induced the entry of Ca in ECs via the EC-expressed TRPM2. Prevention of generation of adenosine diphosphoribose in ECs significantly reduced Ca entry in response to PMN activation of TRPM2 in ECs. PMNs isolated from mice significantly reduced Ca entry in ECs via TRPM2 as compared with wild-type PMNs and failed to induce PMN transmigration. Overexpression of the adenosine diphosphoribose insensitive TRPM2 mutant channel (C1008→A) in ECs suppressed the Ca entry response. Further, the forced expression of TRPM2 mutant channel (C1008→A) or silencing of poly ADP-ribose polymerase in ECs of mice prevented PMN transmigration. CONCLUSIONS: Thus, endotoxin-induced transmigration of PMNs was secondary to TRPM2-activated Ca signaling and VE-cadherin phosphorylation resulting in the disassembly of adherens junctions and opening of the paracellular pathways. These results suggest blocking TRPM2 activation in ECs is a potentially important means of therapeutically modifying PMN-mediated vascular inflammation.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Ativação de Neutrófilo/fisiologia
Neutrófilos/metabolismo
Canais de Cátion TRPM/biossíntese
Migração Transendotelial e Transepitelial/fisiologia
Lesões do Sistema Vascular/metabolismo
[Mh] Termos MeSH secundário: Animais
Movimento Celular/fisiologia
Células Cultivadas
Células Endoteliais/patologia
Expressão Gênica
Seres Humanos
Pulmão/irrigação sanguínea
Pulmão/metabolismo
Pulmão/patologia
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Canais de Cátion TRPM/genética
Lesões do Sistema Vascular/genética
Lesões do Sistema Vascular/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TRPM Cation Channels); 0 (TRPM2 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.311747


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[PMID]:28771621
[Au] Autor:Pazos MA; Lanter BB; Yonker LM; Eaton AD; Pirzai W; Gronert K; Bonventre JV; Hurley BP
[Ad] Endereço:Mucosal Immunology & Biology Research Center, Massachusetts General Hospital for Children, Boston, Massachusetts, United States of America.
[Ti] Título:Pseudomonas aeruginosa ExoU augments neutrophil transepithelial migration.
[So] Source:PLoS Pathog;13(8):e1006548, 2017 Aug.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excessive neutrophil infiltration of the lungs is a common contributor to immune-related pathology in many pulmonary disease states. In response to pathogenic infection, airway epithelial cells produce hepoxilin A3 (HXA3), initiating neutrophil transepithelial migration. Migrated neutrophils amplify this recruitment by producing a secondary gradient of leukotriene B4 (LTB4). We sought to determine whether this two-step eicosanoid chemoattractant mechanism could be exploited by the pathogen Pseudomonas aeruginosa. ExoU, a P. aeruginosa cytotoxin, exhibits phospholipase A2 (PLA2) activity in eukaryotic hosts, an enzyme critical for generation of certain eicosanoids. Using in vitro and in vivo models of neutrophil transepithelial migration, we evaluated the impact of ExoU expression on eicosanoid generation and function. We conclude that ExoU, by virtue of its PLA2 activity, augments and compensates for endogenous host neutrophil cPLA2α function, leading to enhanced transepithelial migration. This suggests that ExoU expression in P. aeruginosa can circumvent immune regulation at key signaling checkpoints in the neutrophil, resulting in exacerbated neutrophil recruitment.
[Mh] Termos MeSH primário: Proteínas de Bactérias/imunologia
Leucotrieno B4/imunologia
Infiltração de Neutrófilos/imunologia
Infecções por Pseudomonas/imunologia
Migração Transendotelial e Transepitelial/imunologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Neutrófilos/imunologia
Pseudomonas aeruginosa/patogenicidade
Virulência/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (pseudomonas exoprotein A protein, Pseudomonas aeruginosa); 1HGW4DR56D (Leukotriene B4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006548


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[PMID]:28754798
[Au] Autor:Veenstra M; Williams DW; Calderon TM; Anastos K; Morgello S; Berman JW
[Ad] Endereço:Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA.
[Ti] Título:Frontline Science: CXCR7 mediates CD14 CD16 monocyte transmigration across the blood brain barrier: a potential therapeutic target for NeuroAIDS.
[So] Source:J Leukoc Biol;102(5):1173-1185, 2017 Nov.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD14 CD16 monocytes transmigrate into the CNS of HIV-positive people in response to chemokines elevated in the brains of infected individuals, including CXCL12. Entry of these cells leads to viral reservoirs, neuroinflammation, and neuronal damage. These may eventually lead to HIV-associated neurocognitive disorders. Although antiretroviral therapy (ART) has significantly improved the lives of HIV-infected people, the prevalence of cognitive deficits remains unchanged despite ART, still affecting >50% of infected individuals. There are no therapies to reduce these deficits or to prevent CNS entry of CD14 CD16 monocytes. The goal of this study was to determine whether CXCR7, a receptor for CXCL12, is expressed on CD14 CD16 monocytes and whether a small molecule CXCR7 antagonist (CCX771) can prevent CD14 CD16 monocyte transmigration into the CNS. We showed for the first time that CXCR7 is on CD14 CD16 monocytes and that it may be a therapeutic target to reduce their entry into the brain. We demonstrated that CD14 CD16 monocytes and not the more abundant CD14 CD16 monocytes or T cells transmigrate to low homeostatic levels of CXCL12. This may be a result of increased CXCR7 on CD14 CD16 monocytes. We showed that CCX771 reduced transmigration of CD14 CD16 monocytes but not of CD14 CD16 monocytes from uninfected and HIV-infected individuals and that it reduced CXCL12-mediated chemotaxis of CD14 CD16 monocytes. We propose that CXCR7 is a therapeutic target on CD14 CD16 monocytes to limit their CNS entry, thereby reducing neuroinflammation, neuronal damage, and HIV-associated neurocognitive disorders. Our data also suggest that CCX771 may reduce CD14 CD16 monocyte-mediated inflammation in other disorders.
[Mh] Termos MeSH primário: Terapia Antirretroviral de Alta Atividade
Fatores Imunológicos/farmacologia
Receptores de Lipopolissacarídeos/imunologia
Receptores CXCR/antagonistas & inibidores
Receptores de IgG/imunologia
Migração Transendotelial e Transepitelial/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Astrócitos/efeitos dos fármacos
Astrócitos/imunologia
Astrócitos/virologia
Barreira Hematoencefálica/imunologia
Barreira Hematoencefálica/patologia
Barreira Hematoencefálica/virologia
Contagem de Linfócito CD4
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/virologia
Disfunção Cognitiva/tratamento farmacológico
Disfunção Cognitiva/imunologia
Disfunção Cognitiva/prevenção & controle
Disfunção Cognitiva/virologia
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/imunologia
Células Endoteliais/virologia
Feminino
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/imunologia
Expressão Gênica
Infecções por HIV/tratamento farmacológico
Infecções por HIV/imunologia
Infecções por HIV/prevenção & controle
Infecções por HIV/virologia
HIV-1/efeitos dos fármacos
HIV-1/crescimento & desenvolvimento
Seres Humanos
Receptores de Lipopolissacarídeos/genética
Masculino
Meia-Idade
Modelos Biológicos
Monócitos/efeitos dos fármacos
Monócitos/imunologia
Monócitos/virologia
Cultura Primária de Células
Receptores CXCR/genética
Receptores CXCR/imunologia
Receptores de IgG/genética
Migração Transendotelial e Transepitelial/genética
Migração Transendotelial e Transepitelial/imunologia
Carga Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCR7 protein, human); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (Immunologic Factors); 0 (Lipopolysaccharide Receptors); 0 (Receptors, CXCR); 0 (Receptors, IgG)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3HI0517-167R


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Texto completo
[PMID]:28739875
[Au] Autor:Resheq YJ; Menzner AK; Bosch J; Tickle J; Li KK; Wilhelm A; Hepburn E; Murihead G; Ward ST; Curbishley SM; Zimmermann HW; Bruns T; Gilbert DF; Tripal P; Mackensen A; Adams DH; Weston CJ
[Ad] Endereço:Institute of Immunology and Immunotherapy, Centre for Liver Research and National Institute for Health Research Birmingham Liver Biomedical Research Centre, College of Medicine and Dentistry, University of Birmingham, Edgbaston, Birmingham B15 2TT, United Kingdom; yazid.resheq@uk-erlangen.de.
[Ti] Título:Impaired Transmigration of Myeloid-Derived Suppressor Cells across Human Sinusoidal Endothelium Is Associated with Decreased Expression of CD13.
[So] Source:J Immunol;199(5):1672-1681, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human monocytic myeloid-derived suppressor cells (MO-MDSCs) within the hepatic compartment suppress inflammation and impair immune surveillance in liver cancer. It is currently not known whether recruitment of MO-MDSCs from blood via hepatic sinusoidal endothelium (HSEC) contributes to their enrichment within the hepatic compartment. We compared the transmigratory potential of MO-MDSCs and monocytes after adhesion to hepatic endothelial monolayers in flow-based assays that mimic in vivo shear stress in the sinusoids. Despite comparable binding to HSEC monolayers, proportionally fewer MO-MDSCs underwent transendothelial migration, indicating that the final steps of extravasation, where actin polymerization plays an important role, are impaired in MO-MDSCs. In this article, we found reduced levels of CD13 on MO-MDSCs, which has recently been reported to control cell motility in monocytes, alongside reduced VLA-4 expression, an integrin predominantly involved in adherence to the apical side of the endothelium. CD13 and VLA-4 blocking and activating Abs were used in flow-based adhesion assays, live-cell imaging of motility, and actin polymerization studies to confirm a role for CD13 in impaired MO-MDSC transmigration. These findings indicate that CD13 significantly contributes to tissue infiltration by MO-MDSCs and monocytes, thereby contributing to the pathogenesis of hepatic inflammation.
[Mh] Termos MeSH primário: Antígenos CD13/metabolismo
Epitélio Posterior/fisiologia
Hemocromatose/imunologia
Hepatite/imunologia
Fígado/imunologia
Células Supressoras Mieloides/imunologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Actinas/metabolismo
Anticorpos Bloqueadores/farmacologia
Antígenos CD13/genética
Antígenos CD13/imunologia
Adesão Celular
Movimento Celular
Células Cultivadas
Regulação para Baixo
Seres Humanos
Integrina alfa4beta1/genética
Integrina alfa4beta1/imunologia
Integrina alfa4beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Antibodies, Blocking); 0 (Integrin alpha4beta1); EC 3.4.11.2 (CD13 Antigens)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600466



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