The Effect of Bacterial Toxins on Platelet Function

Kerrigan, Steven W.; Cox, Dermot

doi:10.1007/978-90-481-9295-3_36

Cited by 3 publications

(4 citation statements)

References 118 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While direct interactions of bacteria with platelets are critical in the subsequent platelet activation, bacteria also secrete many products including toxins that have the potential to interact with platelets ( 130 ). S. aureus secretes a number of substances that have been shown to activate platelets including extracellular adherence protein Eap, chemotaxis inhibitory protein of S. aureus (CHIPS), formyl peptide receptor-like 1 inhibitory protein (FLIPr) and the autolysin Atl ( 131 ).…”

Section: Interactions Of Secreted Bacterial Products With Plateletsmentioning

confidence: 99%

“…There is also a family of pore-forming toxins that act like the calcium ionophore (A23187) ( 133 ). These include pneumolysin ( S. pneumonia ), Streptolysin O (Group A streptococci) and α-toxin ( S. aureus ) ( 130 ). Shiga toxin is produced by some strains of E. coli and plays an important role in the pathogenesis of haemolytic uremic syndrome (HUS).…”

Section: Interactions Of Secreted Bacterial Products With Plateletsmentioning

confidence: 99%

See 1 more Smart Citation

Sepsis – it is all about the platelets

Cox

2023

Front. Immunol.

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Interactions Of Secreted Bacterial Products With Plateletsmentioning

confidence: 99%

Section: Interactions Of Secreted Bacterial Products With Plateletsmentioning

confidence: 99%

Sepsis – it is all about the platelets

Cox

2023

Front. Immunol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…As well as interacting with platelets through surface proteins, bacteria can secrete toxins that can activate platelets [73]. Porphyromonas gingivalis is an oral pathogen that secretes a family of cysteine proteases known as gingipains [74].…”

Section: Platelet Receptorsmentioning

confidence: 99%

Platelets and the innate immune system: mechanisms of bacterial‐induced platelet activation

Cox

Kerrigan

Watson

2011

Journal of Thrombosis and Haemostasis

266

254

View full text Add to dashboard Cite

Summary. It has become clear that platelets are not simply cell fragments that plug the leak in a damaged blood vessel; they are, in fact, also key components in the innate immune system, which is supported by the presence of Toll‐like receptors (TLRs) on platelets. As the cells that respond first to a site of injury, they are well placed to direct the immune response to deal with any resulting exposure to pathogens. The response is triggered by bacteria binding to platelets, which usually triggers platelet activation and the secretion of antimicrobial peptides. The main platelet receptors that mediate these interactions are glycoprotein (GP)IIb–IIIa, GPIbα, FcγRIIa, complement receptors, and TLRs. This process may involve direct interactions between bacterial proteins and the receptors, or can be mediated by plasma proteins such as fibrinogen, von Willebrand factor, complement, and IgG. Here, we review the variety of interactions between platelets and bacteria, and look at the potential for inhibiting these interactions in diseases such as infective endocarditis and sepsis.

show abstract

“…In contrast Staphylococcus aureus binds fibrinogen, which in turn binds to GPIIb/IIIa on the platelet surface. S. aureus also produces toxins that activate platelets [17]. For the majority of bacteria that activate platelets, binding of IgG is required.…”

Section: Introductionmentioning

confidence: 99%