Platelet Interactions with Bacteria

Kerrigan, Steven W.

doi:10.5772/60531

Cited by 4 publications

(3 citation statements)

References 92 publications

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“…Bacteria interact with platelets through three main mechanisms: (i) by direct binding: bacteria can express surface proteins which allow them to interact directly with surface receptors on platelets and bind to them, as in the case of Streptococcus sanguinis , which showed the ability to bind directly to GPIbα [ 3 ]; (ii) by binding through plasma proteins: bacterial proteins are capable of binding to fibrinogen and vWF (von Willebrand Factor), serving as a bridge between two cells, as in the example of Staphylococcus aureus expressing surface protein A (SpA) that binds to vWf and which in turn binds to platelet GPIbα [ 4 ]; (iii) and by binding through the secretion of bacterial products, such as toxins, which interact with platelets and activate them. Among these molecules, the Shiga toxin secreted by Escherichia coli induces platelet aggregation by binding to glycosphingolipid receptors on the surface of platelets [ 5 , 6 , 7 , 8 , 9 , 10 ]. This difference in interaction mechanisms, which is mainly dependent on the bacteria, induces distinct platelet responses.…”

Section: Introductionmentioning

confidence: 99%

The Antibacterial Effect of Platelets on Escherichia coli Strains

et al. 2022

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Platelets play an important role in defense against pathogens; however, the interaction between Escherichia coli and platelets has not been well described and detailed. Our goal was to study the interaction between platelets and selected strains of E. coli in order to evaluate the antibacterial effect of platelets and to assess bacterial effects on platelet activation. Washed platelets and supernatants of pre-activated platelets were incubated with five clinical colistin-resistant and five laboratory colistin-sensitive strains of E. coli in order to study bacterial growth. Platelet activation was measured with flow cytometry by evaluating CD62P expression. To identify the difference in strain behavior toward platelets, a pangenome analysis using Roary and O-antigen serotyping was carried out. Both whole platelets and the supernatant of activated platelets inhibited growth of three laboratory colistin-sensitive strains. In contrast, platelets promoted growth of the other strains. There was a negative correlation between platelet activation and bacterial growth. The Roary results showed no logical clustering to explain the mechanism of platelet resistance. The diversity of the responses might be due to strains of different types of O-antigen. Our results show a bidirectional interaction between platelets and E. coli whose expression is dependent on the bacterial strain involved.

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Section: Introductionmentioning

confidence: 99%

The Antibacterial Effect of Platelets on Escherichia coli Strains

et al. 2022

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“…Staphylococcus aureus can bind to platelets directly by fibrinogen and/or fibronectin, which are ligands for GPIIb-IIIa and/or via a short amino acid sequence, arginyl glycyl aspartic acid. 64 Protein A exposed on the surface of bacteria Staphylococcus aureus can attach to the FcγRII receptor exposed on the surface of platelet membrane and can lead to the release of serotonin and platelet aggregation. Both FcγRII, required for Staphylococcus aureus adhesion, and aggregation induced by these bacteria depend on FcγRII, which activates GPIIb-IIIa functions.…”

Section: Interaction Of Platelets With Bacteriamentioning

confidence: 99%

“…67 However, in binding to platelet, bacteria most often use an IgG molecule that interacts with the FcγRIIa platelet receptor. 64 Binding of bacteria to platelets leads to their aggregation, as shown in the example of Streptococcus sanguinis, Staphylococcus epidermidis, or Chlamydia pneumoniae. 9 Many bacteria ie gram-positive bacteria Staphylococcus aureus can activate the blood clotting system and influence the individual coagulation factors, although they do not lead directly to the initiation of the coagulation cascade.…”

Section: Interaction Of Platelets With Bacteriamentioning

confidence: 99%

<p>Microbial Modulation of Coagulation Disorders in Venous Thromboembolism</p>

Lichota

Gwoździński

Szewczyk

2020

JIR

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Venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), is the third leading cause of cardiovascular death in the world. Important risk factors of thrombosis include bed restraint, surgery, major trauma, long journeys, inflammation, pregnancy, and oral contraceptives, previous venous thromboembolism, cancer, and bacterial infections. Sepsis increases the risk of blood clot formation 2-20 times. In this review, we discussed various mechanisms related to the role of bacteria in venous thrombosis also taking into consideration the role of the human microbiome. Many known bacteria, such as Helicobacter pylori, Chlamydia pneumoniae, Mycoplasma pneumoniae, Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus, and Escherichia coli, causing infections may increase the risk of thrombotic complications through platelet activation or may lead to an inflammatory reaction involving the fibrinolytic system. Additionally, the bacteria participate in the production of factors causing or increasing the risk of cardiovascular diseases. An example can be trimethylamine N-oxide (TMAO) but also uremic toxins (indoxyl sulfate), short-chain fatty acids (SCFA) phytoestrogens, and bile acids. Finally, we presented the involvement of many bacteria in the development of venous thromboembolism and other cardiovascular diseases.

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