5 research outputs found
Prominent Role Of Platelets In The Formation Of Circulating Neutrophil-red Cell Heterocellular Aggregates In Sickle Cell Anemia
[No abstract available]9911e214e217Hidalgo, A., Chang, J., Jang, J.E., Peired, A.J., Chiang, E.Y., Frenette, P.S., Heterotypic interactions enabled by polarized neutrophil microdomains mediate thromboinflammatory injury (2009) Nat Med, 15 (4), pp. 384-391Turhan, A., Jenab, P., Bruhns, P., Ravetch, J.V., Coller, B.S., Frenette, P.S., Intravenous immune globulin prevents venular vaso-occlusion in sickle cell mice by inhibiting leukocyte adhesion and the interactions between sickle erythrocytes and adherent leukocytes (2004) Blood, 103 (6), pp. 2397-2400Turhan, A., Weiss, L.A., Mohandas, N., Coller, B.S., Frenette, P.S., Primary role for adherent leukocytes in sickle cell vascular occlusion: A new paradigm (2002) Proc Natl Acad Sci USA, 99 (5), pp. 3047-3051May, A.E., Langer, H., Seizer, P., Bigalke, B., Lindemann, S., Gawaz, M., Platelet-leukocyte interactions in inflammation and atherothrombosis (2007) Semin Thromb Hemost, 33 (2), pp. 123-127Gawaz, M., Fateh-Moghadam, S., Pilz, G., Gurland, H.J., Werdan, K., Platelet activation and interaction with leucocytes in patients with sepsis or multiple organ failure (1995) Eur J Clin Invest, 25 (11), pp. 843-851Polanowska-Grabowska, R., Wallace, K., Field, J.J., Chen, L., Marshall, M.A., Figler, R., P-selectin-mediated platelet-neutrophil aggregate formation activates neutrophils in mouse and human sickle cell disease (2010) Art Thromb Vascular Biol, 30 (12), pp. 2392-2399Brittain, J.E., Knoll, C.M., Ataga, K.I., Orringer, E.P., Parise, L.V., Fibronectin bridges monocytes and reticulocytes via integrin alpha4beta1 (2008) Br J Haematol, 141 (6), pp. 872-881Chaar, V., Picot, J., Renaud, O., Bartolucci, P., Nzouakou, R., Bachir, D., Aggregation of mononuclear and red blood cells through an {alpha}4{beta}1-Lu/basal cell adhesion molecule interaction in sickle cell disease (2010) Haematologica, 95 (11), pp. 1841-1848Finnegan, E.M., Turhan, A., Golan, D.E., Barabino, G.A., Adherent leukocytes capture sickle erythrocytes in an in vitro flow model of vasoocclusion (2007) Am J Hematol, 82 (4), pp. 266-275Wun, T., Paglieroni, T., Tablin, F., Welborn, J., Nelson, K., Cheung, A., Platelet activation and platelet-erythrocyte aggregates in patients with sickle cell anemia (1997) J Lab Clin Med, 129 (5), pp. 507-516Hynes, R.O., Integrins: Versatility, modulation, and signaling in cell adhesion (1992) Cell, 69 (1), pp. 11-25Novelli, E.M., Kato, G.J., Ragni, M.V., Zhang, Y., Hildesheim, M.E., Nouraie, M., Plasma thrombospondin-1 is increased during acute sickle cell vaso-occlusive events and associated with acute chest syndrome, hydroxyurea therapy, and lower hemolytic rates (2012) Am J Hematol, 87 (3), pp. 326-330Proenca-Ferreira, R., Brugnerotto, A.F., Garrido, V.T., Dominical, V.M., Vital, D.M., Ribeiro Mde, F., Endothelial activation by platelets from sickle cell anemia patients (2014) PloS one, 9 (2)Kutlar, A., Ataga, K.I., McMahon, L., Howard, J., Galacteros, F., Hagar, W., A potent oral P-selectin blocking agent improves microcirculatory blood flow and a marker of endothelial cell injury in patients with sickle cell disease (2012) Am J Hematol, 87 (5), pp. 536-539Telen, M.J., Wun, T., McCavit, T.L., De Castro, L.M., Krishnamurti, L., Lanzkron, S., GMI 1070: Reduction In Time To Resolution Of Vaso-Occlusive Crisis and Decreased Opioid Use In a Prospective, Randomized, Multi-Center Double Blind, Adaptive Phase 2 Study In Sickle Cell Disease (2013) Blood, 122 (21), p. 7. , Abstrac
In vitro microfluidic model for the study of vaso-occlusive processes
Vaso-occlusion, responsible for much of the morbidity of sickle-cell disease, is a complex multicellular process, apparently triggered by leukocyte adhesion to the vessel wall. The microcirculation represents a major site of leukocyte-endothelial interactions and vaso-occlusive processes. We have developed a biochip with subdividing interconnecting microchannels that decrease in size (40 μm to 10 μm in width), for use in conjunction with a precise microfluidic device, to mimic cell flow and adhesion through channels of sizes that approach those of the microcirculation. The biochips were utilized to observe the dynamics of the passage of neutrophils and red blood cells, isolated from healthy and sickle-cell anemia (SCA) individuals, through laminin or endothelial adhesion molecule-coated microchannels at physiologically relevant rates of flow and shear stress. Obstruction of E-selectin/intercellular adhesion molecule 1-coated biochip microchannels by SCA neutrophils was significantly greater than that observed for healthy neutrophils, particularly in the microchannels of 40-15 μm in width. Whereas SCA red blood cells alone did not significantly adhere to, or obstruct, microchannels, mixed suspensions of SCA neutrophils and red blood cells significantly adhered to and obstructed laminin-coated channels. Results from this in vitro microfluidic model support a primary role for leukocytes in the initiation of SCA occlusive processes in the microcirculation. This assay represents an easy-to-use and reproducible in vitro technique for understanding molecular mechanisms and cellular interactions occurring in subdividing microchannels of widths approaching those observed in the microvasculature. The assay could hold potential for testing drugs developed to inhibit occlusive mechanisms such as those observed in SCA and thrombotic diseases.Vaso-occlusion, responsible for much of the morbidity of sickle-cell disease, is a complex multicellular process, apparently triggered by leukocyte adhesion to the vessel wall. The microcirculation represents a major site of leukocyte-endothelial interact43223228FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO2010/17320-0; 2010/18386-4565036/01
Neutrophils Of Rheumatoid Arthritis Patients On Anti-tnf-α Therapy And In Disease Remission Present Reduced Adhesive Functions In Association With Decreased Circulating Neutrophil-attractant Chemokine Levels
Neutrophils participate in the initiation and progression of rheumatoid arthritis (RA) although the exact mechanisms responsible for neutrophil accumulation in rheumatoid joints are not understood. This study compared the adhesive and chemotactic functions of neutrophils from RA patients in activity (DAS28>3.2) and not in activity (DAS28<2.6) and observed the effects of different treatment approaches on these functions. Neutrophils were isolated from healthy controls (CON), and patients with active or inactive RA in use of therapy not specific for RA (NSAIDs), in use of DMARDs and in use of anti-TNF-α therapy. Adhesive and chemotactic properties were evaluated using in vitro assays; adhesion molecule expression was assessed by flow cytometry and real-time PCR and circulating chemokines were determined by ELISA. No significant alterations in the adhesive and chemotactic properties of neutrophils from active RA were observed when compared to CON neutrophils, independently of treatment regimen. In contrast, neutrophils from RA patients in disease remission presented reduced adhesive properties and a lower spontaneous chemotactic capacity, in association with decreased adhesion molecule expression, although profiles of alterations differed for those patients on DMARDs and those on anti-TNF-α therapy. Circulating levels of the major neutrophilic chemokines, IL-8 and epithelial neutrophil activating peptide-78, were also significantly decreased in those patients demonstrating a clinical response. Remission of RA appears to be associated with ameliorations in aspects important for neutrophil adhesion and chemotaxis; whether these alterations contribute to decrease neutrophil migration to the synovial fluid, with consequent improvements in the clinical manifestations of RA, remains to be determined. © 2011 The Authors. 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Interactions of sickle red blood cells with neutrophils are stabilized on endothelial cell layers
sem informação5613840FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO2010/18386-4; 10/17320-