Blockade of glycoprotein IIb/IIIa by crotavirin, a member of disintegrins, prevents platelet from activation and aggregation by Staphylococcus aureus bacteria

Chao Zong Liu, Hsin Yi Huang, Pei-Jane Tsai, Mei Hsu Shih

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Interaction with circulating platelets is considered an important virulent mechanism for Staphylococcus aureus (S. aureus) bacteria to induce endocarditis, a severe infectious disease with high incidence of systemic thrombosis. It therefore represents an important target for pharmacological intervention. In this study, we found that the clinical isolate S. aureus 30326 induced activation and aggregation of washed human platelets in a fibrinogen-dependent manner and this platelet reactivity was abrogated by crotavirin, a snake venom-derived glycoprotein (GP) IIb/IIIa antagonist, indicating that crotavirin is able to protect platelets from activation and aggregation by S. aureus 30326. When tested at a concentration that prevented the platelet reactivity of S. aureus 30326, crotavirin also interfered with the binding of bacteria to washed human platelets supplemented with fibrinogen. The fibrinogen-binding activity of S. aureus has been shown to be essential for S. aureus to trigger platelet activation and aggregation. Crotavirin failed to affect the fibrinogen binding of S. aureus 30326 and neither did it bind to this microbe, suggesting that the inhibitory action of crotavirin on the S. aureus 30326-platelet interaction resulted from the occupation of platelet GPIIb/IIIa. Taken together, these results demonstrate an important role for GPIIb/IIIa in mediating the interaction of platelets with S. aureus in the presence of fibrinogen and platelet GPIIb/IIIa thus appears to be a new target for the intervention of S. aureus-platelet interaction.

Original languageEnglish
Pages (from-to)145-155
Number of pages11
JournalThrombosis Research
Volume116
Issue number2
DOIs
Publication statusPublished - 2005 Jun 6

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Disintegrins
Platelet Glycoprotein GPIIb-IIIa Complex
Platelet Activation
Platelet Aggregation
Staphylococcus aureus
Blood Platelets
Bacteria
Fibrinogen
crotavirin
Snake Venoms
Endocarditis
Occupations
Communicable Diseases
Thrombosis
Pharmacology

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Hematology

Cite this

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title = "Blockade of glycoprotein IIb/IIIa by crotavirin, a member of disintegrins, prevents platelet from activation and aggregation by Staphylococcus aureus bacteria",
abstract = "Interaction with circulating platelets is considered an important virulent mechanism for Staphylococcus aureus (S. aureus) bacteria to induce endocarditis, a severe infectious disease with high incidence of systemic thrombosis. It therefore represents an important target for pharmacological intervention. In this study, we found that the clinical isolate S. aureus 30326 induced activation and aggregation of washed human platelets in a fibrinogen-dependent manner and this platelet reactivity was abrogated by crotavirin, a snake venom-derived glycoprotein (GP) IIb/IIIa antagonist, indicating that crotavirin is able to protect platelets from activation and aggregation by S. aureus 30326. When tested at a concentration that prevented the platelet reactivity of S. aureus 30326, crotavirin also interfered with the binding of bacteria to washed human platelets supplemented with fibrinogen. The fibrinogen-binding activity of S. aureus has been shown to be essential for S. aureus to trigger platelet activation and aggregation. Crotavirin failed to affect the fibrinogen binding of S. aureus 30326 and neither did it bind to this microbe, suggesting that the inhibitory action of crotavirin on the S. aureus 30326-platelet interaction resulted from the occupation of platelet GPIIb/IIIa. Taken together, these results demonstrate an important role for GPIIb/IIIa in mediating the interaction of platelets with S. aureus in the presence of fibrinogen and platelet GPIIb/IIIa thus appears to be a new target for the intervention of S. aureus-platelet interaction.",
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Blockade of glycoprotein IIb/IIIa by crotavirin, a member of disintegrins, prevents platelet from activation and aggregation by Staphylococcus aureus bacteria. / Liu, Chao Zong; Huang, Hsin Yi; Tsai, Pei-Jane; Shih, Mei Hsu.

In: Thrombosis Research, Vol. 116, No. 2, 06.06.2005, p. 145-155.

Research output: Contribution to journalArticle

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