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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.
Infection and Immunity
|February 1, 1992
Summary
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.