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Human platelet aggregation by Yersinia pseudotuberculosis is mediated by invasin
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.