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Marc E. De Broe - One of the best experts on this subject based on the ideXlab platform.
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anti b7 1 blocks Mononuclear Cell adherence in vasa recta after ischemia
Kidney International, 2001Co-Authors: Kathleen E De Greef, Dirk Ysebaert, Samuel Dauwe, Sven R Vercauteren, Veerle P. Persy, Marc E. De BroeAbstract:Anti-B7-1 blocks Mononuclear Cell adherence in vasa recta after ischemia. Background Blocking the costimulatory pathway by CTLA-4 Ig, reactive with both B7-1 and B7-2 costimulatory molecules, protects the kidney during acute ischemia/reperfusion injury. This study investigated whether and how B7-1 and/or B7-2 proteins are involved in renal ischemia/reperfusion injury (IRI). Methods Uninephrectomized rats were submitted to warm renal ischemia (30 min) and received control monoclonal antibody (mAb; 17E3), anti-B7-1 (3H5), anti-B7-2 (24F), a combination of anti-B7-1/B7-2, or CTLA-4 Ig. Renal function, morphology, and the kinetics of inflammatory Cells were studied for a ten-day period. Binding sites of the injected antibodies were detected by secondary staining with anti-mouse Ab. Results Compared with controls, acute renal failure (ARF) in the anti-B7-1 group was attenuated both functionally and morphologically. Anti-B7-1/B7-2 and CTLA-4 Ig also were protective in IRI. ARF was not altered by anti-B7-2 treatment. Two hours after reperfusion, B7-1 was expressed along the endothelial Cells of the ascending vasa recta. Expression of B7-1 increased over time during the first 24 hours and decreased thereafter. Two hours after reperfusion, adherence/accumulation of T Cells and monocytes/macrophages was found in the vasa recta of the ischemic kidney. Anti-B7-1–treated animals had fewer T Cells and monocytes/macrophages in the vasa recta compared with controls. Leukocyte accumulation in these vessels after anti-B7-2 treatment was not different from IRI controls. Conclusion These observations strongly support the key role of the B7-1 protein in the protection of renal IRI through inhibition of T Cell and monocyte adherence at the level of the ascending vasa recta.
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anti b7 1 blocks Mononuclear Cell adherence in vasa recta after ischemia
Kidney International, 2001Co-Authors: Kathleen E De Greef, Dirk Ysebaert, Samuel Dauwe, Sven R Vercauteren, Veerle P. Persy, Marc E. De BroeAbstract:Anti-B7-1 blocks Mononuclear Cell adherence in vasa recta after ischemia. Background Blocking the costimulatory pathway by CTLA-4 Ig, reactive with both B7-1 and B7-2 costimulatory molecules, protects the kidney during acute ischemia/reperfusion injury. This study investigated whether and how B7-1 and/or B7-2 proteins are involved in renal ischemia/reperfusion injury (IRI). Methods Uninephrectomized rats were submitted to warm renal ischemia (30 min) and received control monoclonal antibody (mAb; 17E3), anti-B7-1 (3H5), anti-B7-2 (24F), a combination of anti-B7-1/B7-2, or CTLA-4 Ig. Renal function, morphology, and the kinetics of inflammatory Cells were studied for a ten-day period. Binding sites of the injected antibodies were detected by secondary staining with anti-mouse Ab. Results Compared with controls, acute renal failure (ARF) in the anti-B7-1 group was attenuated both functionally and morphologically. Anti-B7-1/B7-2 and CTLA-4 Ig also were protective in IRI. ARF was not altered by anti-B7-2 treatment. Two hours after reperfusion, B7-1 was expressed along the endothelial Cells of the ascending vasa recta. Expression of B7-1 increased over time during the first 24 hours and decreased thereafter. Two hours after reperfusion, adherence/accumulation of T Cells and monocytes/macrophages was found in the vasa recta of the ischemic kidney. Anti-B7-1–treated animals had fewer T Cells and monocytes/macrophages in the vasa recta compared with controls. Leukocyte accumulation in these vessels after anti-B7-2 treatment was not different from IRI controls. Conclusion These observations strongly support the key role of the B7-1 protein in the protection of renal IRI through inhibition of T Cell and monocyte adherence at the level of the ascending vasa recta.
Soraia C. Abreu - One of the best experts on this subject based on the ideXlab platform.
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bone marrow Mononuclear Cell therapy in experimental allergic asthma intratracheal versus intravenous administration
Respiratory Physiology & Neurobiology, 2013Co-Authors: Soraia C. Abreu, Tatiana Marongutierrez, Fernanda F. Cruz, Debora S. Ornellas, Mariana A. Antunes, Adriana L Silva, Bruno L Diaz, Alexandre Muxfeldt Absaber, Vera Luiza Capelozzi, Debora G. XistoAbstract:Abstract We hypothesized that the route of administration would impact the beneficial effects of bone marrow-derived Mononuclear Cell (BMDMC) therapy on the remodelling process of asthma. C57BL/6 mice were randomly assigned to two main groups. In the OVA group, mice were sensitized and challenged with ovalbumin, while the control group received saline using the same protocol. Twenty-four hours before the first challenge, control and OVA animals were further randomized into three subgroups to receive saline (SAL), BMDMCs intravenously (2 × 10 6 ), or BMDMCs intratracheally (2 × 10 6 ). The following changes were induced by BMDMC therapy in OVA mice regardless of administration route: reduction in resistive and viscoelastic pressures, static elastance, eosinophil infiltration, collagen fibre content in airways and lung parenchyma; and reduction in the levels of interleukin (IL)-4, IL-13, transforming growth factor-β and vascular endothelial growth factor. In conclusion, BMDMC modulated inflammatory and remodelling processes regardless of administration route in this experimental model of allergic asthma.
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Protective effects of bone marrow Mononuclear Cell therapy on lung and heart in an elastase-induced emphysema model
Respiratory Physiology & Neurobiology, 2012Co-Authors: Fernanda F. Cruz, Debora G. Xisto, Lívia C. Fujisaki, Johnatas D. Silva, Tatiana Maron-gutierrez, Debora S. Ornellas, Soraia C. Abreu, Mariana A. Antunes, Nazareth N. RochaAbstract:Abstract We hypothesized that bone marrow-derived Mononuclear Cell (BMDMC) therapy protects the lung and consequently the heart in experimental elastase-induced emphysema. Twenty-four female C57BL/6 mice were intratracheally instilled with saline (C group) or porcine pancreatic elastase (E group) once a week during 4 weeks. C and E groups were randomized into subgroups receiving saline (SAL) or male BMDMCs (2 × 10 6 , Cell) intravenously 3 h after the first saline or elastase instillation. Compared to E-SAL group, E-Cell mice showed, at 5 weeks: lower mean linear intercept, neutrophil infiltration, elastolysis, collagen fiber deposition in alveolar septa and pulmonary vessel wall, lung Cell apoptosis, right ventricle wall thickness and area, higher endothelial growth factor and insulin-like growth factor mRNA expressions in lung tissue, and reduced platelet-derived growth factor, transforming growth factor-β, and caspase-3 expressions. In conclusion, BMDMC therapy was effective at modulating the inflammatory and remodeling processes in the present model of elastase-induced emphysema.
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bone marrow Mononuclear Cell therapy led to alveolar capillary membrane repair improving lung mechanics in endotoxin induced acute lung injury
Cell Transplantation, 2010Co-Authors: Luiz Felipe M Prota, Roberta M Lassance, Tatiana Marongutierrez, C S N B Garcia, Maria Cristina E Santana, Vivian Yochiko Samoto, Raquel C Castiglione, Jackson Souzamenezes, Soraia C. Abreu, Marcelo Felipe SantiagoAbstract:The aim of this study was to test the hypothesis that bone marrow Mononuclear Cell (BMDMC) therapy led an improvement in lung mechanics and histology in endotoxin-induced lung injury. Twenty-four C57BL/6 mice were randomly divided into four groups (n = 6 each). In the acute lung injur;y (ALI) group, Escherichia coli lipopolysaccharide (LPS) was instilled intratracheally (40 µg, IT), and control (C) mice received saline (0.05 ml, IT). One hour after the administration of saline or LPS, BMDMC (2 × 107 Cells) was intravenously injected. At day 28, animals were anesthetized and lung mechanics [static elastance (Est), resistive (∆P1), and viscoelastic (∆P2) pressures] and histology (light and electron microscopy) were analyzed. Immunogold electron microscopy was used to evaluate if multinucleate Cells were type II epithelial Cells. BMDMC therapy prevented endotoxin-induced lung inflammation, alveolar collapse, and interstitial edema. In addition, BMDMC administration led to epithelial and endothelial repair with multinucleated type II pneumocytes. These histological changes yielded a reduction in lung Est, ∆P1, and ∆P2 compared to ALI. In the present experimental ALI model, the administration of BMDMC yielded a reduction in the inflammatory process and a repair of epithelium and endothelium, reducing the amount of alveolar collapse, thus leading to an improvement in lung mechanics.
Kathleen E De Greef - One of the best experts on this subject based on the ideXlab platform.
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anti b7 1 blocks Mononuclear Cell adherence in vasa recta after ischemia
Kidney International, 2001Co-Authors: Kathleen E De Greef, Dirk Ysebaert, Samuel Dauwe, Sven R Vercauteren, Veerle P. Persy, Marc E. De BroeAbstract:Anti-B7-1 blocks Mononuclear Cell adherence in vasa recta after ischemia. Background Blocking the costimulatory pathway by CTLA-4 Ig, reactive with both B7-1 and B7-2 costimulatory molecules, protects the kidney during acute ischemia/reperfusion injury. This study investigated whether and how B7-1 and/or B7-2 proteins are involved in renal ischemia/reperfusion injury (IRI). Methods Uninephrectomized rats were submitted to warm renal ischemia (30 min) and received control monoclonal antibody (mAb; 17E3), anti-B7-1 (3H5), anti-B7-2 (24F), a combination of anti-B7-1/B7-2, or CTLA-4 Ig. Renal function, morphology, and the kinetics of inflammatory Cells were studied for a ten-day period. Binding sites of the injected antibodies were detected by secondary staining with anti-mouse Ab. Results Compared with controls, acute renal failure (ARF) in the anti-B7-1 group was attenuated both functionally and morphologically. Anti-B7-1/B7-2 and CTLA-4 Ig also were protective in IRI. ARF was not altered by anti-B7-2 treatment. Two hours after reperfusion, B7-1 was expressed along the endothelial Cells of the ascending vasa recta. Expression of B7-1 increased over time during the first 24 hours and decreased thereafter. Two hours after reperfusion, adherence/accumulation of T Cells and monocytes/macrophages was found in the vasa recta of the ischemic kidney. Anti-B7-1–treated animals had fewer T Cells and monocytes/macrophages in the vasa recta compared with controls. Leukocyte accumulation in these vessels after anti-B7-2 treatment was not different from IRI controls. Conclusion These observations strongly support the key role of the B7-1 protein in the protection of renal IRI through inhibition of T Cell and monocyte adherence at the level of the ascending vasa recta.
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anti b7 1 blocks Mononuclear Cell adherence in vasa recta after ischemia
Kidney International, 2001Co-Authors: Kathleen E De Greef, Dirk Ysebaert, Samuel Dauwe, Sven R Vercauteren, Veerle P. Persy, Marc E. De BroeAbstract:Anti-B7-1 blocks Mononuclear Cell adherence in vasa recta after ischemia. Background Blocking the costimulatory pathway by CTLA-4 Ig, reactive with both B7-1 and B7-2 costimulatory molecules, protects the kidney during acute ischemia/reperfusion injury. This study investigated whether and how B7-1 and/or B7-2 proteins are involved in renal ischemia/reperfusion injury (IRI). Methods Uninephrectomized rats were submitted to warm renal ischemia (30 min) and received control monoclonal antibody (mAb; 17E3), anti-B7-1 (3H5), anti-B7-2 (24F), a combination of anti-B7-1/B7-2, or CTLA-4 Ig. Renal function, morphology, and the kinetics of inflammatory Cells were studied for a ten-day period. Binding sites of the injected antibodies were detected by secondary staining with anti-mouse Ab. Results Compared with controls, acute renal failure (ARF) in the anti-B7-1 group was attenuated both functionally and morphologically. Anti-B7-1/B7-2 and CTLA-4 Ig also were protective in IRI. ARF was not altered by anti-B7-2 treatment. Two hours after reperfusion, B7-1 was expressed along the endothelial Cells of the ascending vasa recta. Expression of B7-1 increased over time during the first 24 hours and decreased thereafter. Two hours after reperfusion, adherence/accumulation of T Cells and monocytes/macrophages was found in the vasa recta of the ischemic kidney. Anti-B7-1–treated animals had fewer T Cells and monocytes/macrophages in the vasa recta compared with controls. Leukocyte accumulation in these vessels after anti-B7-2 treatment was not different from IRI controls. Conclusion These observations strongly support the key role of the B7-1 protein in the protection of renal IRI through inhibition of T Cell and monocyte adherence at the level of the ascending vasa recta.
Liliane Dalcortivo - One of the best experts on this subject based on the ideXlab platform.
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bone marrow derived Mononuclear Cell therapy induces distal angiogenesis after local injection in critical leg ischemia
Modern Pathology, 2008Co-Authors: David M Smadja, Jeanpaul Duong Van Huyen, Patrick Bruneval, Pascale Gaussem, Liliane DalcortivoAbstract:Critical leg ischemia is associated with a high risk of amputation when revascularization is not possible. Cell therapy based on bone marrow-derived Mononuclear Cells or with peripheral Mononuclear Cells, collected after stimulation with G-CSF has been used in an attempt to stimulate angiogenesis. Although several studies have raised the hope that such Cell therapy may be effective in critical leg ischemia, no direct demonstration of angiogenesis induced by bone marrow-derived Mononuclear Cell/peripheral Mononuclear Cell injection has been reported in man. The aim of this study was to identify and to evaluate the extent of the angiogenic process associated with Cell therapy in critical leg ischemia in man. To address this question, this pathological study was conducted in patients enrolled in the OPTIPEC clinical trial (Optimization of Progenitor Endothelial Cells in the Treatment of Critical leg ischemia), an interventional Cell therapy study in critical leg ischemia. Amputation specimens from these patients were submitted to a standardized dissection protocol. In three patients, an active angiogenesis was observed in the distal part of the ischemic limb but not in the gastrocnemius muscle, the site of bone marrow Cell injection. All the newly formed vessels were positive for endothelial Cell markers (CD31, CD34, von Willebrand factor) and negative for markers of lymphatic vessels (podoplanin). Immunohistochemical staining for Ki-67 and c-kit showed extensive endothelial Cell proliferation within the new vessels. Bone marrow-derived Mononuclear Cell therapy in patients with critical leg ischemia induces an active, substained angiogenesis in the ischemic and distal parts of the treated limb, although this may not prevent amputation in some patients with very severe ischemia.
Marcelo Felipe Santiago - One of the best experts on this subject based on the ideXlab platform.
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bone marrow Mononuclear Cell therapy led to alveolar capillary membrane repair improving lung mechanics in endotoxin induced acute lung injury
Cell Transplantation, 2010Co-Authors: Luiz Felipe M Prota, Roberta M Lassance, Tatiana Marongutierrez, C S N B Garcia, Maria Cristina E Santana, Vivian Yochiko Samoto, Raquel C Castiglione, Jackson Souzamenezes, Soraia C. Abreu, Marcelo Felipe SantiagoAbstract:The aim of this study was to test the hypothesis that bone marrow Mononuclear Cell (BMDMC) therapy led an improvement in lung mechanics and histology in endotoxin-induced lung injury. Twenty-four C57BL/6 mice were randomly divided into four groups (n = 6 each). In the acute lung injur;y (ALI) group, Escherichia coli lipopolysaccharide (LPS) was instilled intratracheally (40 µg, IT), and control (C) mice received saline (0.05 ml, IT). One hour after the administration of saline or LPS, BMDMC (2 × 107 Cells) was intravenously injected. At day 28, animals were anesthetized and lung mechanics [static elastance (Est), resistive (∆P1), and viscoelastic (∆P2) pressures] and histology (light and electron microscopy) were analyzed. Immunogold electron microscopy was used to evaluate if multinucleate Cells were type II epithelial Cells. BMDMC therapy prevented endotoxin-induced lung inflammation, alveolar collapse, and interstitial edema. In addition, BMDMC administration led to epithelial and endothelial repair with multinucleated type II pneumocytes. These histological changes yielded a reduction in lung Est, ∆P1, and ∆P2 compared to ALI. In the present experimental ALI model, the administration of BMDMC yielded a reduction in the inflammatory process and a repair of epithelium and endothelium, reducing the amount of alveolar collapse, thus leading to an improvement in lung mechanics.
