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La hexoquinasa es un receptor inmune innato para la detección del peptidoglicano bacteriano
Andrea J Wolf1, Christopher N Reyes2, Wenbin Liang3
1F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Cell
|July 5, 2016
Resumen
Las bacterias Gram positivas activan el inflamatorio NLRP3 a través de la N-acetilglucosamina, detectada por la enzima metabólica hexoquinasa. Este hallazgo revela una enzima metabólica que actúa como un receptor de reconocimiento de patrones, impactando las respuestas inmunes.
Área de la Ciencia:
- Inmunología
- Biología celular
- El metabolismo
Sus antecedentes:
- El inflamatorio NLRP3 (NLRP3) media las respuestas inflamatorias, incluyendo la secreción de interleucina (IL) - 1β y IL-18.
- La degradación del peptidoglicano en los fagosomas típicamente activa las vías inflamatorias a través del reconocimiento NOD2 del dipeptido muramil.
- Los mecanismos precisos que vinculan los componentes bacterianos a la activación de NLRP3 siguen siendo un área activa de investigación.
Objetivo del estudio:
- Elucidar el mecanismo por el cual la degradación del peptidoglicano bacteriano Gram-positivo activa el inflamatorio NLRP3.
- Identificar el componente bacteriano específico y el sensor huésped involucrados en esta vía de activación del inflamatorio NLRP3.
- Investigar el papel de las enzimas metabólicas en el reconocimiento de patrones inmunológicos innatos.
Principales métodos:
- Se ha investigado la activación del inflamatorio NLRP3 en respuesta a los productos de degradación del peptidoglicano.
- Utilizó la inhibición de la N-acetilglucosamina y la hexokinasa como herramientas experimentales.
- Examinó la localización de la hexoquinasa en las membranas externas mitocondriales.
- Se evaluó el impacto de los inhibidores glicolíticos y las condiciones metabólicas en la activación del inflamatorio.
Principales resultados:
- La activación del inflamatorio NLRP3 es provocada por la liberación de N-acetilglucosamina a partir del peptidoglicano.
- La enzima glucolítica hexoquinasa actúa como el sensor citosólico para la N-acetilglucosamina.
- La inhibición de la hexoquinasa por la N-acetilglucosamina conduce a su disociación de las mitocondrias, suficiente para la activación de NLRP3.
- Las condiciones metabólicas y los inhibidores glicolíticos que afectan a la hexoquinasa también inducen la activación del inflamatorio.
Conclusiones:
- Una enzima metabólica, la hexoquinasa, funciona como un receptor de reconocimiento de patrones para la N-acetilglucosamina.
- Esta vía representa un nuevo mecanismo para la activación del inflamatorio NLRP3 distinto de la señalización NOD2.
- El estudio destaca la interacción entre el metabolismo del huésped y el reconocimiento de patrones inmunológicos innatos.
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