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Papel de la escisión de C3 en la activación de monocitos durante la circulación extracorpórea
C S Rinder1, H M Rinder, K Johnson
1Department of Laboratory Medicine and Anesthesiology, Yale University School of Medicine, New Haven, CT 06520-8035, USA. christine.rinder@yale.edu
Circulation
|August 3, 1999
Resumen
El bloqueo de la activación temprana del complemento, específicamente C3a, evita la activación de los monocitos durante la circulación extracorpórea simulada (SECC). Esto contrasta con hallazgos anteriores en los que solo la inhibición del complemento terminal bloqueaba la activación de las plaquetas y los neutrófilos.
Área de la Ciencia:
- Inmunología Inmunología.
- El bypass cardiopulmonar es un procedimiento de derivación por vía bypass cardiopulmonar.
- El sistema de complemento es un sistema de complemento.
Sus antecedentes:
- Estudios anteriores mostraron que la inhibición del complemento terminal (C5a, C5b-9) bloqueaba la activación de plaquetas y neutrófilos, pero no la activación de monocitos durante la SECC.
- Este estudio investigó si la inhibición anterior del complemento, mediante el bloqueo de C3a, podría prevenir la activación de los monocitos.
Objetivo del estudio:
- Para determinar si el bloqueo de la formación de C3a durante la SECC previene la activación de monocitos.
- Para comprender mejor la relación entre la activación del complemento y la activación de las células sanguíneas durante el bypass cardiopulmonar simulado.
Principales métodos:
- Modelo de circulación extracorpórea simulada (SECC) utilizando sangre humana y un oxigenador de membrana.
- Administración de CAB-2, una proteína quimérica que inhibe las convertasas C3/C5, para bloquear la formación de C3a, C5a y C5b-9.
- Los ensayos para los componentes del complemento (C3a, C5b-9), la activación de los monocitos (CD11b), la activación de los neutrófilos (CD11b, elastasa) y la activación de las plaquetas (P-selectina, conjugados).
Principales resultados:
- CAB-2 inhibió significativamente la formación de C3a y C5b-9 en ambas dosis probadas.
- Las dosis altas de CAB-2 bloquearon significativamente la regulación ascendente de los monocitos y los neutrófilos CD11b y la liberación de la elastasa en los neutrófilos.
- CAB-2 también inhibió la formación de conjugados monocito-plaquetarios dependientes de la activación plaquetaria.
Conclusiones:
- El bloqueo temprano del complemento (inhibición de C3a) impidió la regulación ascendente de los monocitos CD11b durante la SECC.
- Los componentes del complemento temprano son cruciales para la activación de los monocitos en el SECC.
- Este estudio aclara el papel del sistema del complemento en la activación de las células sanguíneas durante el bypass cardiopulmonar simulado.
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