Investigation of platelet–neutrophil interactions in whole blood by flow cytometry

Peters, Mark; Heyderman, R S; Hatch, D. J.; Klein, Nigel

doi:10.1016/s0022-1759(97)00139-7

Cited by 59 publications

(49 citation statements)

References 24 publications

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“…8,12 PNC, forming as a result of the interaction of platelet P-selectin and neutrophils also promotes platelet activation. 24 This is the first study to demonstrate that P-selectin and PNC were significantly correlated with arterial stiffness evaluated by PWV in normal subjects. In an analysis of four randomized trials, Hebert et al 29 showed that aspirin therapy was beneficial in the primary prevention of vascular disease.…”

Section: Discussionmentioning

confidence: 74%

“…Sample preparation and measurement of platelet P-selectin (CD62P) and PNC levels were performed according to the method described by Peters et al 24 To minimize platelet activation during blood collection, blood was drawn via a 21 G butterfly needle without the use of a tourniquet. After discarding the first 2 ml of blood, a further 2 ml was collected and immediately added to 200 ml of sodium citrate (3.13%).…”

Section: Measurement Of Platelet Activationmentioning

confidence: 99%

“…2,3,5,9,10,12 Furthermore, detection of platelet-neutrophil complexes (PNC), which are formed as a result of interaction with CD62P provides an additional means to detect platelet activation. 24 The purpose of this study was to investigate the association between arterial stiffness and platelet activation by measuring PWV, P-selectin, and PNC in subjects without atherosclerotic disease.…”

Section: Introductionmentioning

confidence: 99%

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Association between arterial stiffness and platelet activation

Yamasaki¹,

Furuno

Satō

et al. 2005

J Hum Hypertens

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Increased arterial stiffness is strongly associated with atherosclerosis, while platelet activation is an important trigger of thrombotic events in patients with atherosclerosis. However, little is known about the effect of arterial stiffness on platelet activation. We therefore investigated the association between arterial stiffness and platelet activation in 38 normal volunteers (20 men and 18 women) aged 23-77 years (mean ¼ 49715 years). Arterial stiffness was assessed by measuring brachialankle pulse wave velocity (ba-PWV) and heart-brachial PWV (hb-PWV). Flow cytometric analyses were performed to evaluate platelet activation by measuring surface expression of P-selectin and platelet-neutrophil complexes (PNC) before and after activation by ADP. We also calculated the difference between basal and stimulated states of P-selectin and PNC to assess platelet activation reserve. PWVs were significantly correlated with age and BP (r ¼ 0.60-0.81). For platelet activation and activation reserve, correlations with age were less strong but remained significant (r ¼ 0.36-0.61), with the exception of P-selectin (not significant, NS), and correlations with SBP were similar (r ¼ 0.35-0.53). A significant correlation was found between PWVs and platelet activation (r ¼ 0. 43-0.74). Multiple regression analysis demonstrated significant correlations between platelet activation and reserve and PWVs (coefficient ¼ 2.17-6.59), when both age and BP were adjusted for simultaneously. In conclusion, platelet activation was associated with arterial stiffness, suggesting that arterial stiffness may play an important role in thrombotic events.

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Section: Discussionmentioning

confidence: 74%

Section: Measurement Of Platelet Activationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association between arterial stiffness and platelet activation

Yamasaki¹,

Furuno

Satō

et al. 2005

J Hum Hypertens

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“…Circulating platelets bind to neutrophils, and platelet-neutrophil complexes have been demonstrated in whole blood (Rinder et al, 1991). Such a satellitism, already described in 1974 (Kjeldsberg and Swanson, 1974), may have potent pathophysiologic relevance because at rest, 25% of blood neutrophils are complexed with platelets, and after platelet activation with ADP or thrombin, such complexes rise to 70% (Peters et al, 1997). Besides their phlogogenic activity through interactions with neutrophils, platelets can counterbalance neutrophil activation.…”

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confidence: 90%

Platelets Abrogate Leukotriene B4 Generation by Human Blood Neutrophils Stimulated with Monosodium Urate Monohydrate or f-Met-Leu-Phe In Vitro

Chabannes

Poubelle

Molière

et al. 2003

Laboratory Investigation

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SUMMARY:Neutrophils are physiologically associated with platelets in whole blood. Inflammatory reactions can be modulated by the presence of platelets. To investigate the influence of platelets on neutrophil activity, we studied the 5-lipoxygenase (5-LOX) metabolic pathway in normal human blood neutrophils stimulated with f-Met-Leu-Phe (fMLP) or monosodium urate monohydrate (MSUM) in the presence of autologous platelets. Platelets inhibited by more than 90% the synthesis of leukotriene B 4 and 5-HETE in neutrophils activated with fMLP or MSUM. The addition of exogenous arachidonic acid did not reverse the inhibitory effect of platelets on 5-LOX-generated metabolites in fMLP-or MSUM-activated neutrophils. Preincubation of neutrophils with adenosine deaminase reversed the inhibitory effect of platelets in fMLP-treated neutrophils, indicating that adenosine was responsible for the platelet inhibition of leukotriene B 4 and 5-HETE formation. In contrast, adenosine deaminase had no influence on the inhibitory effects of platelets in MSUM-stimulated cells. These results suggest that platelets can inhibit the synthesis of 5-LOX products (a) by acting mainly downstream to phospholipase A 2 in cells stimulated by fMLP or MSUM, (b) through adenosine when neutrophils are activated with fMLP, and (c) by an adenosine-independent mechanism in MSUM-activated neutrophils by an as-yetunidentified mediator. (Lab Invest 2003, 83:491-499).

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“…There exist conflicting reports on the relative contribution of neutrophil activation to PNC formation. Peters et al have demonstrated that neutrophil activation does not influence PNC formation (5), while other studies have reported that neutrophil activation can decrease complex formation (6). PNC formation has mainly been investigated in disease and is proposed to contribute to the pathogenesis of allergy (7), murine lung injury (8), and sepsis (9,10); however, the importance of these complexes for neutrophil function is not clear.…”

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confidence: 99%

Platelet-Dependent Neutrophil Function Is Dysregulated by M Protein from Streptococcus pyogenes

et al. 2015

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Platelets are rapidly responsive sentinel cells that patrol the bloodstream and contribute to the host response to infection. Platelets have been reported to form heterotypic aggregates with leukocytes and may modulate their function. Here, we have investigated platelet-neutrophil complex formation and neutrophil function in response to distinct agonists. The endogenous platelet activator thrombin gave rise to platelet-dependent neutrophil activation, resulting in enhanced phagocytosis and bacterial killing. Streptococcus pyogenes is an important causative agent of severe infectious disease, which can manifest as sepsis and septic shock. M1 protein from S. pyogenes also mediated platelet-neutrophil complex formation; however, these neutrophils were dysfunctional and exhibited diminished chemotactic ability and bacterial killing. This reveals an important agonist-dependent neutrophil dysfunction during platelet-neutrophil complex formation and highlights the role of platelets during the immune response to streptococcal infection.

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Investigation of platelet–neutrophil interactions in whole blood by flow cytometry

Cited by 59 publications

References 24 publications

Association between arterial stiffness and platelet activation

Association between arterial stiffness and platelet activation

Platelets Abrogate Leukotriene B4 Generation by Human Blood Neutrophils Stimulated with Monosodium Urate Monohydrate or f-Met-Leu-Phe In Vitro

Platelet-Dependent Neutrophil Function Is Dysregulated by M Protein from Streptococcus pyogenes

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