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Daño a la proteína específica del tensioactivo en el síndrome de dificultad respiratoria aguda
C S Baker1, T W Evans, B J Randle
1Cell Biology Unit, National Heart and Lung Institute, Imperial College School of Medicine, London, UK.
Lancet (London, England)
|April 27, 1999
Resumen
El síndrome de dificultad respiratoria aguda (SRAP) daña las proteínas tensioactivas, probablemente a través de la neutrófila elastasa. Este daño in vivo puede limitar la efectividad de las terapias actuales de tensioactivos para pacientes con SDRAR.
Área de la Ciencia:
- Medicina Pulmonar La medicina pulmonar es el tratamiento de las enfermedades pulmonares.
- Cuidados críticos en cuidados intensivos.
- La bioquímica es la bioquímica.
Sus antecedentes:
- El síndrome de dificultad respiratoria aguda (SRAP) es una afección grave con alta mortalidad y sin tratamiento específico.
- La activación de neutrófilos en el SDRAR conduce a lesiones pulmonares y disfunción del tensioactivo.
- La elastasa de los neutrófilos puede degradar las proteínas tensioactivas, lo que podría limitar la eficacia terapéutica.
Objetivo del estudio:
- Para investigar el daño in vivo a las proteínas específicas de los tensioactivos en pacientes con SDRA.
- Para determinar si la neutrófila elastasa es responsable del daño de las proteínas tensioactivas en los pulmones de ARDS.
Principales métodos:
- Se recogieron muestras de tensioactivo pulmonar mediante lavado broncoalveolar de 18 pacientes con ARDS y 6 controles sanos.
- La separación de proteínas se realizó utilizando SDS-PAGE.
- El Western blotting con un anticuerpo monoclonal (E8) identificó la proteína A (SP-A) específica del surfactante.
Principales resultados:
- Catorce de los 18 pacientes con ARDS mostraron evidencia de daño SP-A, distinto de los controles.
- El SP-A dañado exhibió bandas de peso molecular alteradas (55 kDa, 30-36 kDa, 36-40 kDa) en comparación con los dímeros normales (66 kDa) en los controles.
- El patrón de daño observado se parecía a la escisión in vitro de SP-A por la neutrófila elastasa.
Conclusiones:
- Las proteínas específicas de los agentes tensioactivos se dañan directamente en los pulmones de los pacientes con ARDS, probablemente a través de la proteólisis.
- Este daño continuo por los productos neutrófilos puede explicar la respuesta limitada al tensioactivo terapéutico en ARDS.
- La terapia combinada de surfactante y antiproteasa podría ofrecer mejores resultados de tratamiento para el SDRA.
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