Human platelet aggregation by Yersinia pseudotuberculosis is mediated by invasin
Related Experiment Video
Updated: Nov 3, 2026

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
Published on: October 26, 2009
M Simonet1, P Triadou, C Frehel
1Laboratoire de Microbiologie, Faculté de Médecine Necker-Enfants Malades, Paris, France.
Abstract:
Plasmid-free strains of Yersinia pseudotuberculosis induce aggregation of human platelets in vitro. It appears that this phenomenon is mediated by invasin (Inv), a 103-kDa outer membrane protein that permits bacteria to penetrate mammalian cells, since (i) an isogenic inv-deficient mutant failed to aggregate platelets compared with the parental strain; (ii) a monoclonal antibody directed against invasin inhibited platelet aggregation; (iii) Inv+ Escherichia coli HB101 promoted platelet aggregation. Platelet receptors for invasin were identified by using a panel of anti-platelet glycoprotein monoclonal antibodies in a bacterial adhesion assay. We found that bacteria bind to platelet membrane glycoproteins Ic and IIa. Electron microscopic study of bacterium-platelet interactions also revealed that bacteria expressing invasin attach to and are phagocytized by thrombocytes, in contrast to inv-deficient bacteria, indicating that these anucleated cells are able to internalize bacteria in vitro after specific interaction with invasin.
Insights
Yersinia pseudotuberculosis invasin (Inv) protein causes human platelet aggregation and internalization by thrombocytes. This interaction involves platelet glycoproteins Ic and IIa, mediated by bacterial invasin.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Yersinia pseudotuberculosis is a human pathogen.
- Invasin (Inv) is an outer membrane protein mediating bacterial entry into host cells.
- Platelets play a role in immune responses and pathogen interactions.
Purpose of the Study:
- To investigate the role of Yersinia pseudotuberculosis invasin in human platelet aggregation.
- To identify platelet receptors for invasin.
- To examine bacterium-platelet interactions using electron microscopy.
Main Methods:
- Utilized isogenic inv-deficient Yersinia pseudotuberculosis mutants.
- Employed monoclonal antibodies against invasin and platelet glycoproteins.
- Performed bacterial adhesion assays and electron microscopy.
Main Results:
- Plasmid-free Yersinia pseudotuberculosis induced platelet aggregation.
- Invasin-deficient mutants did not aggregate platelets.
- Monoclonal anti-invasin antibodies inhibited aggregation.
- Inv+ Escherichia coli induced aggregation.
- Bacteria adhered to platelet glycoproteins Ic and IIa.
- Invasin-expressing bacteria were phagocytized by platelets.
Conclusions:
- Yersinia pseudotuberculosis invasin mediates platelet aggregation.
- Platelet glycoproteins Ic and IIa are receptors for invasin.
- Platelets can internalize invasin-expressing bacteria via phagocytosis.
Related Concept Videos
Intracellular Movement of Viruses and Bacteria
Cancer Cell Migration through Invadopodia
Intracellular Signaling Affects Focal Adhesions
Some...
Adherens Junctions
Adherens Junctions are Dynamic
The endothelial cells...
Determinants of Bacterial Pathogenicity and Virulence
Plague

