Platelet Activation by Streptococcus pyogenes Leads to Entrapment in Platelet Aggregates, from Which Bacteria Subsequently Escape

Svensson, Lisbeth; Baumgarten, Maria; Mörgelin, Matthias; Shannon, Oonagh

doi:10.1128/iai.02020-14

Cited by 25 publications

(24 citation statements)

References 33 publications

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“…Our finding that the fibrinogen-binding region of the M1 protein is essential to mediate platelet activation and complement activation implies that any released M protein that binds plasma fibrinogen may generate these responses in a susceptible donor with IgG against the M protein. It has previously been demonstrated that at least platelet activation occurs in response to other S. pyogenes serotypes (21,48,49). This underlies the central importance of fibrinogen binding for S. pyogenes pathogenesis.…”

Section: Discussionmentioning

confidence: 97%

Complement Activation Occurs at the Surface of Platelets Activated by Streptococcal M1 Protein and This Results in Phagocytosis of Platelets

Palm

Sjöholm

Malmström

et al. 2019

The Journal of Immunology

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Platelets circulate the bloodstream and principally maintain hemostasis. Disturbed hemostasis, a dysregulated inflammatory state, and a decreased platelet count are all hallmarks of severe invasive Streptococcus pyogenes infection, sepsis. We have previously demonstrated that the released M1 protein from S. pyogenes activates platelets, and this activation is dependent on the binding of M1 protein, fibrinogen, and M1-specific IgG to platelets in susceptible donors. In this study, we characterize the M1-associated protein interactions in human plasma and investigate the acquisition of proteins to the surface of activated platelets and the consequences for platelet immune function. Using quantitative mass spectrometry, M1 protein was determined to form a protein complex in plasma with statistically significant enrichment of fibrinogen, IgG3, and complement components, especially C1q. Using flow cytometry, these plasma proteins were also confirmed to be acquired to the platelet surface, resulting in complement activation on M1-activated human platelets. Furthermore, we demonstrated an increased phagocytosis of M1-activated platelets by monocytes, which was not observed with other physiological platelet agonists. This reveals a novel mechanism of complement activation during streptococcal sepsis, which contributes to the platelet consumption that occurs in sepsis.

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Section: Discussionmentioning

confidence: 97%

Complement Activation Occurs at the Surface of Platelets Activated by Streptococcal M1 Protein and This Results in Phagocytosis of Platelets

Palm

Sjöholm

Malmström

et al. 2019

The Journal of Immunology

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“…This concept has been suggested by the retrieval of viable organisms from platelet-bacterial aggregates in vitro (41). Additionally, there are data suggesting that platelet-bacterial aggregation propagates and protects the development of vegetative lesions in bacterial endocarditis (86, 100, 198). The engulfment of bacteria by platelets appears distinct and less effective than the phagocytic capability of leukocytes (220); the functional consequences of pathogen engulfment by platelets remain to be clearly delineated.…”

Section: Platelets As Immune Cellsmentioning

confidence: 99%

Platelets and Their Interactions with Other Immune Cells

Lam

Vijayan

Rumbaut

2015

Comprehensive Physiology

129

119

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Platelets are anucleate blood cells, long known to be critically involved in hemostasis and thrombosis. In addition to their role in blood clots, increasing evidence reveals significant roles for platelets in inflammation and immunity. However, the notion that platelets represent immune cells is not broadly recognized in the field of Physiology. This manuscript reviews the role of platelets in inflammation and immune responses, and highlights their interactions with other immune cells, including examples of major functional consequences of these interactions.

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“…44 Some bacteria are able to mediate the formation of unstable platelet aggregates from which microbial cells subsequently escape, allowing them to evade host immune responses and disseminate through the circulation during invasive infection. 45 The study of bacteria-platelet interactions only gained momentum in the last 40 years following the publication of a series of papers by Clawson et al [46][47][48][49] Bacteria can interact with platelets via multiple mechanisms and one microorganism may produce several factors capable of interacting with platelets simultaneously. This makes it difficult to study the role of individual receptors.…”

Section: Bacteria-platelet Interactionsmentioning

confidence: 99%

Oral hygiene as a risk factor in infective endocarditis

et al. 2017

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There are many known associations between oral and systemic diseases. This review paper summarizes the proposed mechanisms underlying the links between dental disease and cardiovascular disease before introducing recent research regarding bacteria-platelet interactions. New protein factors have been identified on dental plaque bacteria. One of these, PadA, triggers blood to clot. This research provides new information about how Streptococcus bacteria and platelets interact and could lead to the development of new ways to control the formation of blood clots caused by micro-organisms that access the bloodstream. CPD/Clinical Relevance: This article aims to provide the whole dental team with an overview of bacteria-platelet interactions. This is of particular relevance to infective endocarditis and the recent change in wording to the NICE antibiotic prophylaxis guidelines in the UK.

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Platelet Activation by Streptococcus pyogenes Leads to Entrapment in Platelet Aggregates, from Which Bacteria Subsequently Escape

Cited by 25 publications

References 33 publications

Complement Activation Occurs at the Surface of Platelets Activated by Streptococcal M1 Protein and This Results in Phagocytosis of Platelets

Complement Activation Occurs at the Surface of Platelets Activated by Streptococcal M1 Protein and This Results in Phagocytosis of Platelets

Platelets and Their Interactions with Other Immune Cells

Oral hygiene as a risk factor in infective endocarditis

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