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Los parásitos apicomplejos cooptan a los calpaínos del huésped para facilitar su escape de las células infectadas
Rajesh Chandramohanadas1, Paul H Davis, Daniel P Beiting
1Department of Pharmacology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Science (New York, N.Y.)
|April 4, 2009
Resumen
Los protozoos parásitos como Plasmodium y Toxoplasma usan las proteasas calpain del huésped para escapar. La inhibición de la calpina bloquea la salida de parásitos, mientras que su restauración permite que los parásitos salgan de las células huésped.
Área de la Ciencia:
- Biología celular Biología celular.
- Parasitología Parasitología.
- Biología molecular La biología molecular.
Sus antecedentes:
- Los parásitos del complejo de los simios causan una carga global significativa de enfermedades.
- Estos protozoos se replican intracelularmente y deben salir para propagarse.
Objetivo del estudio:
- Para investigar el papel de las proteasas calpain de las células huésped en la salida de parásitos apicomplejos.
- Para determinar si los calpaínos son esenciales para Plasmodium falciparum y Toxoplasma gondii salga.
Principales métodos:
- Utilizó inmunodepleción, inhibición farmacológica, interferencia de ARN y eliminación genética.
- Empleó enfoques de complementación celular biológica y genética.
- Se estudió la salida de Plasmodium falciparum de los eritrocitos y Toxoplasma gondii de los fibroblastos.
Principales resultados:
- La inhibición o el agotamiento de Calpain-1 bloqueó la salida de Plasmodium falciparum de los eritrocitos.
- Egress fue restaurado con la adición de calpain-1.1, purificado.
- La salida de Toxoplasma gondii fue inhibida por la supresión o eliminación de calpain.
- La complementación genética restauró la salida en ambos modelos de parásitos.
Conclusiones:
- Las calpain proteasas de la célula huésped son cruciales para la salida del parásito del apicomplejo.
- Dirigirse a los calpaines representa una estrategia potencial para inhibir la transmisión de parásitos.
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