Deformation of White Blood Cells Firmly Adhered to Endothelium

2012 ◽  
Author(s):  
Alex C. Szatmary ◽  
Rohan J. Banton ◽  
Charles D. Eggleton
Keyword(s):  
Blood Cells ◽  
Fluid Shear Stress ◽  
White Blood Cells ◽  
Infection Site ◽  
Hydrodynamic Load ◽  
Fluid Shear ◽  
Cell Deformability ◽  
Selectin Ligands ◽  
A Cell ◽  
Bond Kinetics

Circulating white blood cells adhere to endothelium near an infection site; this occurs because infection causes ligands to be expressed on activated endothelium. Initially, a white blood cell rolls on the substrate, but eventually forms a firm adhesion, allowing it to crawl through the endothelial layer toward the infected tissue. A computational model of bond kinetics, cell deformability, and fluid dynamics was used to model the forces experienced by a cell during this process. The cell was modeled as a fluid-filled membrane; on its surface were hundreds of deformable microvilli—little fingers, ruffles in the white blood cell’s wrinkly membrane. These microvilli were deformable and their tips were decorated with PSGL-1 chemical receptors which bound to P-selectin ligands on the surface. Softer cells and cells subjected to higher fluid shear stress deformed more, and having more contact area, they formed more bonds and were able to resist more hydrodynamic load.

scholarly journals The Emerging Role of Neutrophils in the Pathogenesis of Thrombosis in COVID-19

2021 ◽  
Vol 22 (10) ◽  
pp. 5368
Author(s):  
Valeria Iliadi ◽  
Ina Konstantinidou ◽  
Konstantina Aftzoglou ◽  
Sergios Iliadis ◽  
Theocharis G. Konstantinidis ◽  
...  
Keyword(s):  
Blood Cells ◽  
Recent Progress ◽  
Cell Damage ◽  
White Blood Cells ◽  
Mortality Rates ◽  
Neutrophil Extracellular Trap ◽  
High Morbidity ◽  
Infection Site ◽  
Thrombotic Complications

Previous studies have shown that COVID-19 leads to thrombotic complications, which have been associated with high morbidity and mortality rates. Neutrophils are the largest population of white blood cells and play a pivotal role in innate immunity. During an infection, neutrophils migrate from circulation to the infection site, contributing to killing pathogens. This mechanism is regulated by chemokines such as IL-8. Moreover, it was shown that neutrophils play an important role in thromboinflammation. Through a diverse repertoire of mechanisms, neutrophils, apart from directly killing pathogens, are able to activate the formation of thrombi. In COVID-19 patients, neutrophil activation promotes neutrophil extracellular trap (NET) formation, platelet aggregation, and cell damage. Furthermore, neutrophils participate in the pathogenesis of endothelitis. Overall, this review summarizes recent progress in research on the pathogenesis of COVID-19, highlighting the role of the prothrombotic action of neutrophils in NET formation.

Dynamics of a Spherical Capsule in a Near-Wall Shear Flow

2012 ◽  
Author(s):  
Stephanie Nix ◽  
Yohsuke Imai ◽  
Daiki Matsunaga ◽  
Takuji Ishikawa ◽  
Takami Yamaguchi
Keyword(s):  
Blood Cells ◽  
Vessel Wall ◽  
White Blood Cells ◽  
Blood Vessel Wall ◽  
Lateral Migration ◽  
Free Layer ◽  
A Cell ◽  
Spherical Capsule ◽  
Migration Of Cells ◽  
Cell Free Layer

Lateral migration of cells in the bloodstream is affected by the material properties of the constituent cells. In blood vessels, red blood cells migrate to the center of the vessel, leading to the formation of a cell-free layer near the vessel wall; on the other hand, less deformable cells such as white blood cells and platelets are more likely to be found near the blood vessel wall. [1]

scholarly journals Macrophage deformability and phagocytosis

1977 ◽  
Vol 75 (1) ◽  
pp. 185-199 ◽  
Author(s):  
MT Mazur ◽  
Williamson JR
Keyword(s):  
Shear Stress ◽  
Cytochalasin B ◽  
Fluid Shear Stress ◽  
Specific Inhibitor ◽  
Contractile Proteins ◽  
Metabolic Inhibitors ◽  
Atp Content ◽  
Binding Agent ◽  
Fluid Shear ◽  
Cell Deformability

The influence of several metabolic inhibitors and pharmacologic agents on macrophage deformation (induced by fluid shear stress) was examined in relationship to changes in ATP content and phagocytosis of latex beads. Two relatively specific inhibitors of glycolysis (iodoacetate [IA], and sodium fluoride [NaF]) and a sulfhydryl-binding agent (N-ethylmaleimide [NEM] markedly inhibited phagocytosis and reduced cell deformability. A microtubule-disrupting agent (vinblastine) and a highly specific inhibitor of glycolysis (2-deoxyglucose) markedly inhibited phagocytosis without influencing cell deformability. An organomercurial sulfhydryl binding agent p-chloromercuribenzene (PCMBS) and a microfilament-disrupting agent (cytochalasin B) inhibited phagocytosis and increased cell deformability. The effects of these agents on phagocytosis and cell deformability bore no consistent relationship to alterations in cellular content of ATP. The observation that 2-deoxyglucose, the most specific inhibitor of glycolysis examined, reduced ATP content to levels far lower (15 percent of control values) than those achieved by any other agent examined and inhibited phagocytosis without altering cell deformability, suggests that alterations in cell deformability induced by NaF, IA, NEM, PCMBS, and cytochalasin B are not due to inhibition of glycolysis per se, but instead result from direct or indirect effects of these agents on cell constituents, possibly contractile proteins, which are determinants of cell deformability. The finding that cytochalasin B, NEM, PCMBS, and IA interfere with phagocytosis and alter cell deformability, together with evidence that these agents interact with isolated actin and myosin, suggests that contractile proteins are important both in phagocytosis and as determinants of cell deformability. The observation that vinblastine, colchicines, and heavy water (D(2)O) did not alter cell deformability, even though vinblastine caused formation of intracellular crystals of microtubular protein, indicates that microtubules are not major determinants of cell deformability. The observations that beads adhered normally to surfaces of cytochalasin B- and of PCMBS-treated cells and that shear-stress induced deformation was increased whereas phagocytosis was markedly inhibited, suggest that deformation of cells around beads associated with ingestion depends on some form of cellular (contractile?) activity, whereas deformation of cells by fluid shear stress is a passive phenomenon.

scholarly journals A cell-based sensor of fluid shear stress for microfluidics

Lab on a Chip ◽  
2015 ◽  
Vol 15 (6) ◽  
pp. 1563-1573 ◽  
Author(s):  
Sarvesh Varma ◽  
Joel Voldman
Keyword(s):  
Shear Stress ◽  
Fluid Shear Stress ◽  
Flow Conditions ◽  
Fluid Shear ◽  
Nih3t3 Cells ◽  
A Cell ◽  
The Impact

We present a cell-based sensor embedded in NIH3T3 cells that fluoresces upon the application of fluid shear stress (FSS), as a simple and versatile method to assess the impact of various microsystem flow conditions on cell health.

Ultrastructural changes in murine lymphoma cells exposed to ultraviolet-A radiation

1991 ◽  
Vol 49 ◽  
pp. 104-105
Author(s):  
Delma P. Thomas ◽  
Dianne E. Godar
Keyword(s):  
Medical Devices ◽  
Blood Cells ◽  
White Blood Cells ◽  
Consumer Products ◽  
Ultrastructural Changes ◽  
Ultraviolet A ◽  
Uv Spectrum ◽  
Lymphoma Cells ◽  
Murine Lymphoma ◽  
Transmission Electron

Ultraviolet radiation (UVR) from all three waveband regions of the UV spectrum, UVA (320-400 nm), UVB (290-320 nm), and UVC (200-290 nm), can be emitted by some medical devices and consumer products. Sunlamps can expose the blood to a considerable amount of UVR, particularly UVA and/or UVB. The percent transmission of each waveband through the epidermis to the dermis, which contains blood, increases in the order of increasing wavelength: UVC (10%) < UVB (20%) < UVA (30%). To investigate the effects of UVR on white blood cells, we chose transmission electron microscopy to examine the ultrastructure changes in L5178Y-R murine lymphoma cells.

The Effect of Red Blood Cells on the ADP-induced Aggregation of Human Platelets in Flow Through Tubes

1990 ◽  
Vol 63 (01) ◽  
pp. 112-121 ◽  
Author(s):  
David N Bell ◽  
Samira Spain ◽  
Harry L Goldsmith
Keyword(s):  
Platelet Aggregation ◽  
Shear Rate ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Platelet Rich Plasma ◽  
Mean Transit Time ◽  
White Blood Cells ◽  
Aggregate Size ◽  
Human Platelets ◽  
Induced Aggregation

SummaryThe effect of red blood cells, rbc, and shear rate on the ADPinduced aggregation of platelets in whole blood, WB, flowing through polyethylene tubing was studied using a previously described technique (1). Effluent WB was collected into 0.5% glutaraldehyde and the red blood cells removed by centrifugation through Percoll. At 23°C the rate of single platelet aggregtion was upt to 9× greater in WB than previously found in platelet-rich plasma (2) at mean tube shear rates Ḡ = 41.9,335, and 1,920 s−1, and at both 0.2 and 1.0 µM ADP. At 0.2 pM ADP, the rate of aggregation was greatest at Ḡ = 41.9 s−1 over the first 1.7 s mean transit time through the flow tube, t, but decreased steadily with time. At Ḡ ≥335 s−1 the rate of aggregation increased between t = 1.7 and 8.6 s; however, aggregate size decreased with increasing shear rate. At 1.0 µM ADP, the initial rate of single platelet aggregation was still highest at Ḡ = 41.9 s1 where large aggregates up to several millimeters in diameter containing rbc formed by t = 43 s. At this ADP concentration, aggregate size was still limited at Ḡ ≥335 s−1 but the rate of single platelet aggregation was markedly greater than at 0.2 pM ADP. By t = 43 s, no single platelets remained and rbc were not incorporated into aggregates. Although aggregate size increased slowly, large aggregates eventually formed. White blood cells were not significantly incorporated into aggregates at any shear rate or ADP concentration. Since the present technique did not induce platelet thromboxane A2 formation or cause cell lysis, these experiments provide evidence for a purely mechanical effect of rbc in augmenting platelet aggregation in WB.

White blood cells levels and PCOS: direct and indirect relationship with insulin resistance, but not with hyperandogenemia

2013 ◽  
Author(s):  
Olga Papalou ◽  
Sarantis Livadas ◽  
Athanasios Karachalios ◽  
Nektarios Benetatos ◽  
George Boutzios ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Cells ◽  
White Blood Cells ◽  
Indirect Relationship

Endogenous Heparinoids Detected by anti-Xa Activity are Present in Blood during Acute Variceal Bleeding in Cirrhosis. A Prospective Study

2014 ◽  
Vol 23 (2) ◽  
pp. 187-194 ◽  
Author(s):  
Christos Triantos ◽  
Emmanuel Louvros ◽  
Maria Kalafateli ◽  
Anne Riddell ◽  
Ulrich Thalheimer ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Variceal Bleeding ◽  
Blood Cells ◽  
Venous Pressure ◽  
White Blood Cells ◽  
International Normalized Ratio ◽  
Ulcer Bleeding ◽  
Factor X ◽  
Packed Red Blood Cells ◽  
Bacterial Peritonitis

Background & Aims: Endogenous heparinoids have been detected by thromboelastography and quantified by clotting based anti-Xa activity assays in patients with cirrhosis, but their presence in variceal bleeding has not been established yet.Methods: Clotting based anti-Xa activity was measured in A) 30 cirrhotics with variceal bleeding, B) 15 noncirrhotics with peptic ulcer bleeding, C) 10 cirrhotics without infection or bleeding, and D) 10 cirrhotics with hepatocellular carcinoma (HCC).Results: Anti-Xa activity was not detected in ulcer bleeders or in cirrhotics without infection or bleedingbut was present in seven (23%) variceal bleeders (median levels: 0.03 u/mL (0.01-0.07)) and was quantifiable for 3 days in six of seven patients. Four of seven variceal bleeders with anti-Xa activity present had HCC (p=0.023). Age, creatinine, platelet count and total infections the second day from admission were significantly correlated with the presence of measureable anti-Xa levels (p=0.014, 0.032, 0.004 and 0.019, respectively). In the HCC group, anti-Xa activity was present in three patients (30%) [median levels: 0.05 u/mL (0.01-0.06)].Conclusions: In this study, variceal bleeders and 30% of the patients with HCC had endogenous heparinoids that were detected by a clotting based anti-Xa activity assay, whereas there was no anti Xa activity present in patients with cirrhosis without infection, or bleeding or HCC, nor in those with ulcer bleeding. Thus, the anti-Xa activity is likely to be a response to bacterial infection and/or presence of HCC in cirrhosis.List of abbreviations: AFP, alpha-fetoprotein; aPTT, activated partial thromboplastin time; CP, Child-Pugh; FXa, activated factor X; GAGS, glycosaminoglycans; Hb, hemoglobin; HCC, hepatocellular carcinoma; HVPG, hepatic venous pressure gradient; INR, International normalized ratio; LMWHs, low molecular weight heparins; MELD, Model for End-stage Liver Disease; PPP, platelet-poor plasma; PRBC, packed red blood cells; PT, prothrombin time; SBP, sponataneous bacterial peritonitis; TEG, thromboelastography; WBC, white blood cells.

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