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Un circuito de células de tufo activado por metabolitos impulsa la remodelación del intestino delgado
Christoph Schneider1, Claire E O'Leary1, Jakob von Moltke1
1Department of Medicine, University of California San Francisco (UCSF), San Francisco, CA 94143, USA.
Cell
|June 12, 2018
Resumen
El circuito de células del tufo intestinal delgado-ILC2 responde a los parásitos remodelando el intestino. Este circuito, regulado por A20, utiliza la detección de succinato para prevenir nuevas infecciones de helmintos.
Área de la Ciencia:
- Inmunología
- Gastroenterología
- Microbiología
Sus antecedentes:
- El circuito de células del tufo intestinal delgado-ILC2 es crucial para las respuestas epiteliales a los parásitos intestinales.
- Las células de tufo detectan patógenos y activan las células linfoides innatas tipo 2 (ILC2s) a través de IL-25.
- Los ILC2s expresan el receptor IL-25, regulado negativamente por A20 (Tnfaip3).
Objetivo del estudio:
- Investigar el papel de A20 en la regulación del circuito de las células del mechón-ILC2.
- Para aclarar los mecanismos por los cuales este circuito media la remodelación intestinal y la inmunidad.
- Para identificar las señales metabólicas involucradas en la activación del circuito.
Principales métodos:
- Manipulación genética de la A20 en las ILC2.
- Análisis de la morfología del intestino delgado y de las poblaciones de células inmunes.
- Análisis metabólico de la luz intestinal.
- Ensayos funcionales utilizando metabolitos específicos y antagonistas de los receptores.
Principales resultados:
- La deficiencia de A20 en ILC2s activa espontáneamente el circuito de células del tufo-ILC2, lo que lleva al alargamiento y remodelación del intestino delgado.
- La activación del circuito está relacionada con el destete y la colonización por el protista Tritrichomonas, que aumenta el succinato luminal.
- El succinato, detectado por la célula del mechón GPR91, activa las ILC2 a través de una vía dependiente de TRPM5 e IL-25.
- Esta remodelación confiere resistencia a las infecciones secundarias de helmintos, imitando la inmunidad concomitante.
Conclusiones:
- Un circuito de detección metabólico que involucra a las células del mechón y las ILC2 regula la adaptación intestinal y la inmunidad.
- El succinato actúa como un metabolito clave en la activación de este circuito.
- El eje de succinato de células de tufo-ILC2 proporciona resistencia contra nuevas infecciones de helmintos, lo que sugiere un mecanismo evolucionado para manejar los patosimbiontes luminales.
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