scholarly journals Cytoadherence between endothelial cells andP. falciparum infected and noninfected normal and thalassemic red blood cells

2006 ◽  
Vol 70B (6) ◽  
pp. 432-442 ◽  
Author(s):  
P. Butthep ◽  
S. Wanram ◽  
K. Pattanapanyasat ◽  
P. Vattanaviboon ◽  
S. Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Red Blood Cells ◽  
Blood Cells

Phagocytosis of Foreign Red Blood Cells by the Reticulo-Endothelial System

1957 ◽  
Vol 189 (3) ◽  
pp. 520-526 ◽  
Author(s):  
Bernard N. Halpern ◽  
G. Biozzi ◽  
B. Benacerraf ◽  
C. Stiffel
Keyword(s):  
Endothelial Cells ◽  
Red Blood Cells ◽  
Clearance Rate ◽  
Blood Cells ◽  
Red Cell ◽  
Histological Evidence ◽  
Specific Antibodies ◽  
Cell Counts ◽  
India Ink ◽  
Reticulo Endothelial System

The clearance rate of nucleated pigeon erythrocytes injected intravenously into mice and rats has been calculated either by routine differential red cell counts or by measuring the radioactivity of the erythrocytes tagged with P32. Histological evidence is given that the foreign erythrocytes are phagocytized by the reticulo-endothelial cells of the liver and spleen. The clearance rate of the foreign erythrocytes, which measures the speed of the phagocytosis, follows in mice a regular exponential function similar to this previously established for other colloids. No spontaneous antibodies to pigeon erythrocytes could be detected in mice. The rapid and complex clearance rate of pigeon erythrocytes observed in rats is related to the existence of spontaneous specific antibodies. The simultaneous injection of pigeon erythrocytes and of India ink into mice, both phagocytized by the RE cells, results in a competition between the two substances in favor of the smaller particles of carbon.

scholarly journals Fine Structure of the Red Pulp of the Spleen in Hereditary Spherocytosis

Blood ◽  
1972 ◽  
Vol 39 (1) ◽  
pp. 81-98 ◽  
Author(s):  
ZELMA MOLNAR ◽  
HENRY RAPPAPORT
Keyword(s):  
Endothelial Cells ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Hereditary Spherocytosis ◽  
Probable Mechanism ◽  
Hemoglobin Content ◽  
Sinus Endothelial Cells ◽  
In Transit ◽  
Conventional Light Microscopy ◽  
Red Pulp

Abstract The spleens from two children and one adult with hereditary spherocytosis were studied in the electron microscope. Stagnation of the erythrocytes within the splenic cords is attributable to their lack of plasticity as evidenced by the absence of bilobed, tailed, or squeezed forms in transit through the walls of the sinuses. In contrast to the sections studied by conventional light microscopy, the splenic sinuses in hereditary spherocytosis were not "empty," but contained red blood cells, the majority of which had lost their hemoglobin content. Cordal macrophages were increased in all three cases and were abundant in the splenic cords of the adult patient, causing a further impediment to the rapid passage of erythrocytes. Macrophages, and, to a lesser degree, sinus endothelial cells contained the products of hemoglobin breakdown. The macrophages showed active erythrophagocytosis. Sinus endothelial cells rarely contained intact red blood cells, but showed pronounced pinocytotic activity, a probable mechanism of hemoglobin incorporation. Platelets within the endothelial cells of the sinuses were much more frequently seen in the three cases of hereditary spherocytosis than in control spleens. The presence of ferritin in platelets suggests that they too may play a role in clearing the end products of hemolysis from the spleen.

Cell-derived microparticles in haemostasis and vascular medicine

2009 ◽  
Vol 101 (03) ◽  
pp. 439-451 ◽  
Author(s):  
Laurent Burnier ◽  
Pierre Fontana ◽  
Brenda R. Kwak ◽  
Anne Angelillo-Scherrer
Keyword(s):  
Endothelial Cells ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Essential Role ◽  
Cell Types ◽  
Vascular Medicine ◽  
Disease Markers ◽  
Wide Range ◽  
Definition Of ◽  
Different Cell Types

SummaryConsiderable interest for cell-derived microparticles has emerged, pointing out their essential role in haemostatic response and their potential as disease markers, but also their implication in a wide range of physiological and pathological processes. They derive from different cell types including platelets – the main source of microparticles – but also from red blood cells, leukocytes and endothelial cells, and they circulate in blood. Despite difficulties encountered in analyzing them and disparities of results obtained with a wide range of methods, microparticle generation processes are now better understood. However, a generally admitted definition of microparticles is currently lacking. For all these reasons we decided to review the literature regarding microparticles in their widest definition, including ectosomes and exosomes, and to focus mainly on their role in haemostasis and vascular medicine.

No effect of methacrylate-based bone cement CMW 1 on the plasmatic phase of coagulation, red blood cells and endothelial cells in vitro

2001 ◽  
Vol 72 (1) ◽  
pp. 86-93 ◽  
Author(s):  
Elisabetta Cenni ◽  
Gabriela Ciapetti ◽  
Donatella Granchi ◽  
Susanna Stea ◽  
Lucia Savarino ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Red Blood Cells ◽  
Bone Cement ◽  
Blood Cells

scholarly journals Persistence of Chronic Inflammation Despite Years of Transfusion Program in SCD Patients: Changing Red Blood Cells Is Not Sufficient to Treat Sickle Cell Disease

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 764-764
Author(s):  
Abdoul Karim Dembele ◽  
Patricia Hermand-Tournamille ◽  
Florence Missud ◽  
Emmanuelle Lesprit ◽  
Malika Benkerrou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Sickle Cell Disease ◽  
Red Blood Cells ◽  
Chronic Inflammation ◽  
Sickle Cell ◽  
Blood Cells ◽  
Healthy Controls ◽  
Cell Disease ◽  
The Impact

Abstract Sickle cell disease (SCD) is a severe hemoglobinopathy due to abnormal hemoglobin S (HbS). Although red blood cell dysfunction is at the core of the SCD pathophysiology, several studies have highlighted the important role of inflammatory cells like neutrophils. One of the most serious complications of SCD is cerebral vasculopathy (CV), due to the occlusion of one or more intracranial or cervical arteries. In 1998, the STOP study demonstrated that monthly blood transfusions could reduce the risk of stroke by 90% in children with CV. However, there is large heterogeneity in the evolution of CV under chronic transfusion, sometimes requiring exchange transfusion (ET) program for years without succeeding in healing the CV. The aim of the study is to investigate the impact of long-term transfusion program on neutrophil dysfunction, in order to understand if persistent inflammation could contribute to the non-healing of CV despite HbS permanently below 40%. In SCD children undergoing ET program for at least 1 year, we analysed i)the phenotype of neutrophils with 8 markers of activation/adhesion/ageing, ii)the plasmatic levels of elastase, witnessing the NETose activity of neutrophils, and iii)the ex-vivo adhesion of neutrophils on activated endothelial cells. One hundred and two SCD children with an ET transfusion program for at least 6 months because of CV were included in the study. ET session, carried out every 5 weeks and most of the time by erythrapheresis, reached their biological objectives with a mean HbS rate after ET session of 14.1%, and 35.4% before the next ET session, which means that these patients globally live at an average HbS level of 24% for at least 1 year. We managed to limit iron overload with a mean ferritinemia of 207 µg/L in the whole cohort. Despite these satisfactory results in terms of HbS reduction, the efficiency in curing the CV was modest in accordance with the previously described efficiency of ET program in SCD children: after a mean ET program duration of 4.4 years only 22% of them had an improvement of their CV since the beginning of the ET program, while 60% of them had a stagnation of their CV, and 18% of them worsened their vascular lesions. Considering inflammatory parameters, the patients had persistence of high leukocytosis and high neutrophils count (respective mean of 9810 G/L and 5742 G/L), significantly not different of neutrophils count before inclusion in the ET program. In a random subgroup of 20 patients, we analysed neutrophils phenotype, NETose and endothelial adhesion and compared them to healthy controls and SCD children without ET, treated or not with Hydroxyurea (HU). Overall, we observed as expected an activated, aged and adherent profile of neutrophils from untreated SCD children compared to healthy controls, characterized by an overexpression of CD18/CD11b (p=0,03), CD18/CD11a (p=0,02), CD162 (p=0,01), CD66a (p=0,01) and the ageing markers CD184 high/CD62Llow (p=0,04) as well as a higher plasmatic level of elastase (p=0. 01) and higher adhesion of neutrophils to endothelial cells. All these parameters were alleviated in SCD patients treated with HU. In SCD patient undergoing ET program, we found a similar profile of activated neutrophils to that of untreated SCD patients with a similar expression of activation molecules, high level of elastase and the same increase of neutrophils adhesion to endothelial cells compared to controls, witnessing a persistence of chronic inflammation despites years of ET. Overall, our study highlights that the replacement of sickle red blood cells, even for years, is not sufficient to reverse the deleterious inflammatory phenotype of neutrophils. Given the major role of inflammation in endothelial dysfunction, these could contribute to the persistence of CV in a majority of patients despite efficient ET programs. This raises the question of systematically combining ET program with anti-inflammatory treatment such as HU or P-selectin inhibitors in children with CV. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

A Monoclonal Antibody to Lactadherin Inhibits Sickle Red Blood Cell Adhesion to Vascular Endothelial Cells in a Plasma Milieu.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1236-1236
Author(s):  
Swapan K. Dasgupta ◽  
Prasenjit Guchhait ◽  
Anhquyen Le ◽  
Sarvari Yellapragada ◽  
Jose Lopez ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Red Blood Cells ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Blood Cells ◽  
Dependent Manner ◽  
Sickle Erythrocytes ◽  
Sickle Red Blood Cells

Abstract Adherence of red blood cells to the endothelium initiates vaso-occlusion in sickle cell anemia. The increased adhesiveness of sickle erythrocytes is accompanied by several changes in the lipids of the erythrocyte membrane, including increased expression of phosphatidylserine (PS). One important PS-binding protein is lactadherin (also known as milk fat globule-EGF factor 8), a 45-kDa glycoprotein containing an Arg-Gly-Asp (RGD) sequence. It is secreted by macrophages and is present in normal plasma. Lactadherin promotes phagocytosis of PS-expressing apoptotic lymphocytes and sickle red blood cells by anchoring them to integrins on macrophages. Here, we investigated the role of endogenous lactadherin in adhesion of sickle erythrocytes to the endothelium. We developed a murine monoclonal antibody to human lactadherin, called L688, and investigated its effect on the adhesion of sickle red blood cells to histamine-stimulated human umbilical vein endothelial cells under hydrodynamic flow. In three experiments using washed erythrocytes resuspended in autologous plasma from three different patients with sickle cell anemia, L688 (20 μg/ml) inhibited adhesion by 24–30% (p<0.01). Further evidence for an important role for lactadherin in sickle erythrocyte adhesion to endothelial cells was provided by the observation that exogenous lactadherin enhanced adhesion in a concentration-dependent manner. Lactadherin-mediated adhesion was also inhibited by monoclonal antibody abciximab, (c7E3, 10 μg/ml) which targets the β3 integrin subunit common to both αIIbβ3 and αVβ3. Control antibodies had no effect. Finally, the lactadherin-dependent adhesion of sickle erythrocytes to activated endothelium was inhibited by PS vesicles but not by phosphatidylcholine vesicles, confirming an important role for PS in sickle cell adhesion. Consistent with this, normal erythrocytes can be induced to adhere to stimulated HUVEC in a lactadherin-dependent manner by treatment with N-ethylmaleimide (10 mM) and calcium ionophore A23187 (4 μM) — treatment that exposes PS on the outer leaflet of the red cell membrane. Together, these results indicate that lactadherin mediates sickle cell adhesion to the endothelium by bridging PS on the erythrocytes with αVβ3 integrin on the endothelium. We propose that anemia in sickle cell disease is at least partially due to phagocytosis of lactadherin-coated sickle erythrocytes in the spleen, liver, and lymph nodes. Those erythrocytes that are not ingested immediately by macrophages will become more adhesive for endothelium. Thus, lactadherin appears to be involved both in sickle cell clearance from the circulation and in adhesion to endothelium.

Platelet-Independent Adhesion of Red Blood Cells to Von Willebrand Factor

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 2769-2769
Author(s):  
Michel WJ Smeets ◽  
Alexander PJ Vlaar ◽  
Herm Jan M Brinkman ◽  
Jan J Voorberg ◽  
Peter L Hordijk
Keyword(s):  
Endothelial Cells ◽  
Blood Cell ◽  
Red Blood Cells ◽  
Von Willebrand Factor ◽  
Cold Storage ◽  
Blood Cells ◽  
Storage Lesion ◽  
Microparticle Formation ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract Background/Objectives Red blood cell (RBC) transfusion can be lifesaving and is an essential therapy in conditions associated with tissue hypoxia due to anemia. However, recent clinical studies show that both the number of RBCs and the age of RBCs transfused are independent risk factors for an increase in transfusion related morbidity and mortality. It has been suggested that the so called “storage lesion” of RBCs, a reduction of quality of erythrocytes and changes in the erythrocyte concentrate storage medium, is the causal factor. Recently it has been shown that cold storage of erythrocytes induces microparticle formation. These erythrocyte microparticles are pro-coagulant and can cause thrombin formation. Another phenomenon of the storage lesion is the rapid and considerable loss of donor erythrocytes from the circulation of transfused patients. We wondered whether thrombin generated by transfused erythrocyte microparticles could contribute to red blood cell adherence to the vascular endothelium. Cytoadherence of red blood cells could contribute to the loss of circulating transfused red blood cells and vascular obstruction and could explain the observed transfusion associated complications in clinical practice. Methods/Results Employing FACS analysis and a microparticle analyzer we showed that erythrocyte cold storage indeed induces microparticle formation. We confirmed the pro-coagulant properties of these microparticles using a chromogenic substrate specific for thombin and a thrombin-anti-thrombin complex ELISA. To determine whether thrombin could induce adhesion of red blood cells to endothelial cells, we cultured human umbilical vein endothelial cells in micro-perfusion chambers and used live-imaging to define the adherence potential of the erythrocytes to endothelial cells at post-capillary flow rate. Thrombin stimulation of the endothelial cells did increase erythrocyte adhesion to endothelial cells. Moreover, the adhesion of erythrocytes followed a pattern resembling platelets binding to von Willebrand factor (VWF). By using live immunofluoresence imaging we confirmed that the erythrocytes did bind to VWF secreted from endothelial cells. Since erythrocyte-VWF interactions may be mediated by platelets, we used fluorescence cell sorting to remove platelets and erythrocyte-platelet complexes from erythrocyte concentrates. The purified erythrocytes did also bind to VWF secreted by endothelial cells and thereby we confirmed that erythrocytes can bind to VWF in a platelet-independent fashion. We further analyzed the specificity of the erythrocyte-VWF interaction by using different protein coatings in micro-perfusion chambers. Erythrocytes did bind to recombinant high molecular weight VWF multimers. Furthermore, they adhered more potently to VWF when compared to fibrinogen or fibrin but showed little binding to fibronectin, collagen type I, or subendothelial extra-cellular matrix proteins. Conclusion Our results suggest that transfusion of RBCs is able to induce endothelial binding of erythrocytes based on a VWF-erythrocyte interaction. We propose that passive infusion of cold stored erythrocyte derived microparticles promotes thrombin generation which subsequently activates endothelial cells and induces VWF secretion. This results in binding of red blood cells to endothelial cells in a platelet-independent fashion which requires the presence of VWF. Based on our results we hypothesize that binding of erythrocytes to VWF may occlude micro-capillaries thereby contributing to transfusion associated complications. Disclosures No relevant conflicts of interest to declare.

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