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Leishmania immune adherence reaction in vertebrates
1Servicio de Inmunología, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, E-28220 Madrid, Spain.
Parasite Immunology
|April 20, 2001
Summary
Leishmania parasites bind to primate red blood cells, but to platelets in non-primate mammals. This parasite-host cell interaction is an innate immune defense mechanism.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Leishmania parasites are opsonized by C3 complement.
- Immune adherence of C3-opsonized Leishmania to erythrocytes enhances clearance in humans.
- The interaction mechanism in non-primate mammals remains unclear.
Purpose of the Study:
- To investigate the initial host cell interactions of Leishmania in various mammalian species.
- To determine if Leishmania-platelet adherence occurs in non-primate mammals.
- To characterize Leishmania immune adherence as an innate immune mechanism.
Main Methods:
- Studied Leishmania promastigote interaction with erythrocytes from avian and mammalian species.
- Used [111In]-labelled promastigotes.
- Infected ex vivo blood from non-primate mammals (dog, guinea-pig, hamster, mouse, rabbit) with promastigotes.
Main Results:
- Leishmania promastigotes bound only to primate erythrocytes.
- In non-primate mammals, promastigotes rapidly adhered to and formed aggregates with platelets within 1 minute.
- This demonstrates a conserved, yet distinct, initial host cell interaction mechanism.
Conclusions:
- Leishmania-erythrocyte binding is specific to primates.
- Leishmania-platelet binding is the primary interaction in non-primate mammals.
- Leishmania immune adherence represents an innate vertebrate host defense mechanism.