Group G streptococci mediate fibrinogen-dependent platelet aggregation leading to transient entrapment in platelet aggregates

Svensson, Lisbeth; Frick, Inga-Maria; Shannon, Oonagh

doi:10.1099/mic.0.000203

Cited by 5 publications

(3 citation statements)

References 33 publications

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“…Similarly, strains of Streptococcus pyogenes that express fibrinogen-binding M proteins (M1, M3 and M5) can also induce platelet aggregation in a GPIIb/IIIa-dependent manner ( 48 ). Other fibrinogen-binding proteins that mediate platelet aggregation include Sdr G ( Staphylococcus epidermidis ) ( 43 ), SpsL ( Staphylococcus pseudintermedius ) ( 44 , 55 ), and FOG (Group G streptococci) ( 55 ). On the other hand S. aureus secretes extracellular fibrinogen binding protein (Efb) which acts to inhibit platelet aggregation ( 41 ).…”

Section: Pathogen Interaction With Platelet Haemostasis Receptorsmentioning

confidence: 99%

Sepsis – it is all about the platelets

Cox

2023

Front. Immunol.

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Sepsis is accompanied by thrombocytopenia and the severity of the thrombocytopenia is associated with mortality. This thrombocytopenia is characteristic of disseminated intravascular coagulation (DIC), the sepsis-associated coagulopathy. Many of the pathogens, both bacterial and viral, that cause sepsis also directly activate platelets, which suggests that pathogen-induced platelet activation leads to systemic thrombosis and drives the multi-organ failure of DIC. In this paper we review the mechanisms of platelet activation by pathogens and the evidence for a role for anti-platelet agents in the management of sepsis.

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Section: Pathogen Interaction With Platelet Haemostasis Receptorsmentioning

confidence: 99%

Sepsis – it is all about the platelets

Cox

2023

Front. Immunol.

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“…Platelet responses are also altered in other infections syndromes. For example, platelet activation and aggregation are correlated with increased severity of human and experimental sepsis [44,45], clinical and experimental studies shown that infection by Streptococcus induces platelet activation and increased adhesiveness that correlates to a worsening of the inflammatory picture [46].…”

Section: Discussionmentioning

confidence: 99%

Haem oxygenase protects against thrombocytopaenia and malaria-associated lung injury

Azevedo-Quintanilha

Medeiros-de-Moraes

Ferreira

et al. 2020

Malar J

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Background: Malaria-triggered lung injury can occur in both severe and non-severe cases. Platelets may interact with parasitized erythrocytes, leukocytes and endothelium. These interactions can lead to microvessel obstructions and induce release of inflammatory mediators. Induction of the haem oxygenase enzyme is important in the host's response to free haem and to several other molecules generated by infectious or non-infectious diseases. In addition, an important role for the haem oxygenase-1 isotype has been demonstrated in experimental cerebral malaria and in clinical cases. Therefore, the present work aims to determine the influence of haem oxygenase in thrombocytopaenia and acute pulmonary injury during infection with Plasmodium berghei strain NK65. Methods: C57BL/6 mice were infected with P. berghei and analysed 7-10 days post-infection. For each experiment, Cobalt Protoporphyrin IX/CoPPIX or saline were administered. Bronchoalveolar lavage fluid was used for total and differential leukocyte count and for protein measurement. Lungs were used for histological analyses or for analysis of cytokines and western blotting. The lung permeability was analysed by Evans blue dye concentration. Platelet-leukocyte aggregate formation was assayed using the flow cytometer. Results: Plasmodium berghei NK65 infection generated an intense lung injury, with increased levels of inflammatory mediators, oedema, and cell migration into the lung. Plasmodium berghei infection was also accompanied by marked thrombocytopaenia and formation of platelet-leukocyte aggregates in peripheral blood. Treatment with the HO-1 inducer cobalt protoporphyrin IX (CoPPIX) modified the inflammatory response but did not affect the evolution of parasitaemia. Animals treated with CoPPIX showed an improvement in lung injury, with decreased inflammatory infiltrate in the lung parenchyma, oedema and reduced thrombocytopaenia. Conclusion: Data here presented suggest that treatment with CoPPIX inducer leads to less severe pulmonary lung injury and thrombocytopaenia during malaria infection, thus increasing animal survival.

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“…Whereas the role of activation of platelet is crucial on innate immunity, excessive activation of platelets may lead to organ malfunction, and increasing risk of cardiovascular diseases e.g., Infective Endocarditis (IE) [1]. A wide range of microorganism has been investigated for their effect on aggregation [2] of blood platelets, including probiotic lactic acid bacteria such as Lactobacillus [3,4], Escherichia coli [5], Streptococci [6,7], Enterococci [8], Staphylococci [9], Listeria monocytogenes [10], Fusobacterium necrophorum [11,12], Yersinia pseudotuberculosis [13], Aspergillus fumigates [14] and Candida albicans [15]. Previous scientific works have shown an increased incidence of cardiovascular disorders [16] in patients with a history of Gram-positive bacterial infection [17,18].…”

Section: Introductionmentioning

confidence: 99%

The Effect of Probiotic Lactic Acid Bacteria (LAB) Strains on the Platelet Activation: A Flow Cytometry-Based Study

Azizpour¹,

Kessel²,

Oudega³

et al. 2017

J Prob Health

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Platelet-activation and agonist-induced platelet aggregation process to the pathogenesis of Infective Endocarditis (IE), bacteremia symptoms or other thrombotic complications and cardiovascular diseases. Activation of platelets by probiotic lactic acid bacteria strains is considered as thrombotic initiative factor contributing to the development and progression of Lactobacillus endocarditis. The main purpose of the current study was to evaluate the immunologic enhancement effect of probiotic strains L. plantarum, L. acidophilus and L. rhamnosus on the activation of blood platelets. Whole fresh blood flow cytometry was used to measure p-selectin expression and fibrinogen binding at basal levels and following stimulation with platelet agonists and probiotic lactic acid bacteria strains. Platelet activation was determined by labelling with FITC-conjugated anti-human fibrinogen and phycoerythrin (PE)-conjugated anti-human CD62p before analysis by flow cytometry. Thrombin Receptor Activator Peptide-6 (TRAP-6) was used as positive control. The percentage of CD62p-positive platelets, FITC-conjugated and the light scatter profiles of the agonist-activated platelets were used to identify the occurrence and degree of platelet activation. Probiotic lactic acid bacteria strains included in this study did not show any effect on spontaneous activation of human blood platelets. These test strains also failed to exacerbate or diminish the platelet activation property when co-incubated with TRAP-6 platelet agonist. Hence, this is the first in vitro report showing the safety of a group of probiotic lactic acid bacteria in terms of their potential to contribute to the pathogenesis of infective endocarditic (IE), bacteremia symptoms or other thrombotic disorders and correlated cardiovascular complications by initiating the platelet activation.

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Group G streptococci mediate fibrinogen-dependent platelet aggregation leading to transient entrapment in platelet aggregates

Cited by 5 publications

References 33 publications

Sepsis – it is all about the platelets

Sepsis – it is all about the platelets

Haem oxygenase protects against thrombocytopaenia and malaria-associated lung injury

The Effect of Probiotic Lactic Acid Bacteria (LAB) Strains on the Platelet Activation: A Flow Cytometry-Based Study

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