Platelets enhance neutrophil locomotion: evidence for a role of P-selectin

Bengtsson, Torbjörn; Frydén, Aril; Zalavary, Stefan; Whiss, Per A; Orselius, Kristina; Grenegård, Magnus

doi:10.1080/00365519950185463

Cited by 23 publications

(23 citation statements)

References 11 publications

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“…Such data argue for integrin-independent mechanisms. P-selectin promotes the accumulation and emigration of neutrophils during inflammation and thrombosis [16], and its ligand PSGL-1 is probably very important for the early neutrophil activation, including rolling along endothelial P-selectin [36,37]. The results in this study suggest a major contribution of platelet derived components to trigger the P-selectin/PSGL-1 interaction.…”

Section: Discussionmentioning

confidence: 64%

“…It is generally considered that an integrin-mediated firm adhesion of neutrophils to endothelial cells or platelets require a prior selectin-dependent interaction. We have recently found that the presence of adhering platelets markedly enhance both the random and the chemotactic transmigration of neutrophils, and that these effects are mediated by P-selectin and associated with increased expression of complement receptor 3 (CR3, CD18/CD11b, Mac-1 or  M  2 ) [16]. Furthermore, platelets enhance the F c -receptor mediated phagocytosis and respiratory burst in neutrophils [17].…”

Section: Introductionmentioning

confidence: 99%

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Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

2003

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Blood platelets bind rapidly to foreign surfaces and interact with adsorbed proteins and neutrophil granulocytes. We demonstrate by use of luminol-amplified chemiluminescence under stirred and nonstirred conditions that platelets at IgG-coated surfaces amplify the neutrophil extracellular release of reactive oxygen species (ROS). The neutrophil response involved tyrosine phosphorylation, but was only in part induced by neutrophil F c -receptor stimulation. The platelet mediated effects were contact-dependent since the respiratory burst was inhibited when the IgG-stimulated platelets were removed by filtration, but not when they were fixed in paraformaldehyde. Bodipyphallacidin-staining of filamentous actin (F-actin) revealed that an actin-dependent platelet adhesion supported the subsequent adhesion and spreading of neutrophils. The neutrophil ROS-response was lowered when the interaction between platelet P-selectin (CD62P) and neutrophil P-selectin glycoprotein ligand-l (PSGL-1 or CD162) was inhibited. The blocking of L-selectin (CD62L) or blocking of the interaction between platelet glycoprotein (Gp) IIb/IIIa and neutrophil complement receptor 3 (CR3) showed no effect. We conclude that platelet activation on immobilized IgG trigger a contact-dependent "frustrated" phagocytosis by neutrophils, associated with a release of toxic ROS. IgG-stimulated platelets activate neutrophils -Wetterö et al.3

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Section: Discussionmentioning

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

2003

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“…21 Several observations suggest that platelets deposited at sites of thrombosis and vascular injury serve as surrogates for endothelium by recruiting circulating leukocytes. 14,24 Tsuji et al 25 demonstrated that platelet P-selectin directly triggers oxygen radical production in neutrophils, and we have recently shown that collagen-activated platelets stimulate, via P-selectin, leukocyte reactive oxygen species production in whole blood. 26 In addition, raised expression of P-selectin reflects platelet activation involving secretion of a broad range of adhesive proteins, procoagulants, cytokines, and growth factors stored in the ␣-granules.…”

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confidence: 99%

“…16 Several studies indicate that P-selectin mediates adhesion and recruitment of leukocytes to activated platelets, exerts procoagulant activity, and facilitates atherosclerotic development. 14,17 Received In this study, we evaluated the interaction between C pneumoniae and human platelets and found that C pneumoniae binds to platelets and effectively stimulates aggregation, secretion, and surface expression of P-selectin. These observations introduce new possible mechanisms involved in the development of cardiovascular diseases.…”

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confidence: 99%

“…11,12 We have previously reported inflammatory properties of platelets by demonstrating their regulatory effects on leukocyte function. [13][14][15] The ␣-granule constituent P-selectin is considered as a reliable marker of platelet activation and as a predictor of acute coronary heart disease. 16 Several studies indicate that P-selectin mediates adhesion and recruitment of leukocytes to activated platelets, exerts procoagulant activity, and facilitates atherosclerotic development.…”

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confidence: 99%

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Chlamydia pneumoniaeBinds to Platelets and Triggers P-Selectin Expression and Aggregation

Kälvegren

Majeed

Bengtsson

2003

ATVB

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Objective-Evidence linking Chlamydia pneumoniae to atherosclerotic cardiovascular disease is expanding. Platelets are considered to play an essential role in cardiovascular diseases; however, so far platelets have not been associated with an infectious cause of atherosclerosis. This study aims to clarify the interaction between C pneumoniae and platelets and possibly present a novel mechanism in the pathogenesis of atherosclerosis. Methods and Results-The effects of C pneumoniae on platelet aggregation and secretion were assessed with lumiaggregometry, and the ability of C pneumoniae to bind to platelets and stimulate expression of P-selectin was analyzed with flow cytometry. We found that C pneumoniae, at a chlamydia:platelet ratio of 1:15, adheres to platelets and triggers P-selectin expression after 1 minute and causes an extensive aggregation and ATP secretion after 20 minutes of incubation. Inhibition of glycoprotein IIb/IIIa with Arg-Gly-Asp-Ser or abciximab markedly reduced C pneumoniaeinduced platelet aggregation. Exposure of C pneumoniae to polymyxin B, but not elevated temperature, abolished the stimulatory effects on platelet activation, suggesting that chlamydial lipopolysaccharide has an active role. In contrast, other tested bacteria had no or only moderate effects on platelet functions. Key Words: atherosclerosis Ⅲ bacteria-cell interaction Ⅲ LPS Ⅲ thrombosis A therosclerosis and related diseases are a major cause of death in the industrialized world. Differences in the occurrence of typical cardiovascular risk factors, such as smoking, hypertension, and abnormalities of lipid and sugar metabolism, do not explain thoroughly temporal and geographical variations in the prevalence or severity of coronary artery disease. 1 Over the last decade, the potential role of infectious agents in the pathogenesis and progression of atherosclerosis has attracted much attention. 2,3 Among different microorganisms suspected, Chlamydia pneumoniae has arisen as the most plausible pathogen having a causal role. 4 Plaque rupture and thrombosis are the main mechanisms of acute arterial occlusion, leading to myocardial infarction. After taking into account conventional risk factors and genetic predisposition, at least one third of thrombotic incidents remain unclear. Several studies show an association between C pneumoniae and thrombosis in patients with carotid artery disease and venous thromboembolic disease. 5,6 C pneumoniae is an obligate intracellular bacterium responsible for a number of upper and lower respiratory tract diseases in humans, and Ϸ50% of adults worldwide have antibody evidence of previous infection by this bacterium. 7 An association between C pneumoniae infections and atherosclerosis has been demonstrated in a number of epidemiological, serological, immunohistochemical, and molecular biological investigations. 2,8,9 Furthermore, in vitro studies have revealed that C pneumoniae is able to infect and replicate in the major cell types found within the atherosclerotic lesion, such as macrophages, en...

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Oxygen radical production in neutrophils interacting with platelets and surface‐immobilized plasma proteins: Role of tyrosine phosphorylation

Nimeri

Majeed

Elwing

et al. 2003

J Biomedical Materials Res

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The interaction between neutrophil granulocytes and platelets is considered to play an important role in the inflammatory process induced by an implanted foreign material. However, the cellular mechanisms involved remain incompletely understood. We used a luminol-dependent chemiluminescence (CL) technique to analyze the generation of reactive oxygen species (ROS) in human neutrophils interacting with different plasma protein-coated surfaces in the presence or absence of unstimulated or stimulated platelets. The role of tyrosine phosphorylation in the regulation of NADPH oxidase activity was evaluated with quantitative fluorescence microscopy and the specific tyrosine kinase inhibitor genistein. We found that the ROS-production is 2 to 3 times higher in neutrophils on immunoglobulin G (IgG)-coated surfaces than in cells interacting with albumin- or fibrinogen-coated surfaces. Incubation with superoxide dismutase and catalase revealed that about 45% of the ROS was released extracellularly on IgG surfaces whereas corresponding values were 90% and 85% in neutrophils interacting with albumin and fibrinogen, respectively. The presence of platelets markedly increased the extracellular generation of ROS, mainly in neutrophils interacting with IgG- or fibrinogen-coated surfaces whereas the intracellular production was only modestly affected. Quantitative fluorescence microscopy of neutrophils stained with FITC-conjugated anti-phosphotyrosine antibodies showed a correlation between tyrosine phosphorylation, cell spreading, and ROS production. Platelets markedly amplified the anti-phosphotyrosine staining on both fibrinogen- and IgG-coated surfaces whereas the low level of tyrosine phosphorylation in neutrophils on albumin-coated surfaces was not further elevated by platelets. Furthermore, the tyrosine kinase inhibitor genistein inhibited both extra- and intracellular ROS production in neutrophils regardless of the presence of platelets. We demonstrate that plasma protein coating and the presence of platelets are crucial for the inflammatory response of adhering neutrophils and that the oxidative response correlates with the extent of tyrosine phosphorylation of proteins in focal contacts.

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Platelets enhance neutrophil locomotion: evidence for a role of P-selectin

Cited by 23 publications

References 11 publications

Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

Chlamydia pneumoniaeBinds to Platelets and Triggers P-Selectin Expression and Aggregation

Oxygen radical production in neutrophils interacting with platelets and surface‐immobilized plasma proteins: Role of tyrosine phosphorylation

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