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El control del receptor de hidrocarburos de arilo de una vía de defensa de tolerancia a la enfermedad
Alban Bessede1, Marco Gargaro2, Maria T Pallotta3
11] Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy [2] IMS Laboratory, University of Bordeaux, 33607 Pessac, France [3].
Nature
|June 17, 2014
Resumen
La activación del receptor de hidrocarburos de arilo (AhR) por el lipopolisacárido (LPS) inicialmente reduce la inflamación. Esta vía, que involucra a la indoleamina 2,3-dioxigenasa 1 (IDO1) en el retorno, promueve la tolerancia a las endotoxinas y protege contra las infecciones.
Área de la Ciencia:
- Inmunología Inmunología.
- Biología Molecular Biología Molecular
- Interacciones huésped-patógeno.
Sus antecedentes:
- La tolerancia a la enfermedad es crucial para la aptitud del huésped durante la infección.
- La tolerancia a las endotoxinas, un estado de refractividad al lipopolisacárido (LPS), es un aspecto clave de la tolerancia a las enfermedades.
- Comprender los mecanismos de tolerancia a la enfermedad puede revelar nuevas estrategias terapéuticas para las enfermedades inflamatorias.
Objetivo del estudio:
- Para investigar el papel del receptor de hidrocarburos de arilo (AhR) en la tolerancia a las endotoxinas.
- Aclarar los mecanismos moleculares subyacentes a la regulación de la inflamación y la defensa del huésped mediada por AhR.
Principales métodos:
- Los ratones fueron expuestos al LPS para inducir tolerancia.
- Se analizó la activación de AhR y enzimas asociadas como la triptófano 2,3-dioxigenasa y la indoleamina 2,3-dioxigenasa 1 (IDO1).
- Se evaluó el impacto de la señalización AhR en la expresión de genes inflamatorios y la protección contra infecciones bacterianas.
Principales resultados:
- La exposición inicial al LPS activó AhR y la triptófano hepática 2,3-dioxigenasa, regulando a la baja los genes inflamatorios tempranos.
- En el LPS rechallenge, la regulación a largo plazo de la inflamación sistémica mediada por AhR requería indoleamina 2,3-dioxigenasa 1 (IDO1).
- La actividad de la Src quinasa asociada al complejo AhR mejoró la fosforilación y señalización de IDO1, contribuyendo al estado de tolerancia a las endotoxinas.
Conclusiones:
- AhR juega un papel crítico en el establecimiento de la tolerancia a la endotoxina.
- El eje AhR-IDO1 es esencial para la regulación sostenida de la inflamación sistémica y la protección contra las infecciones.
- Los mecanismos de tolerancia a la enfermedad mediados por AhR contribuyen a la aptitud del huésped durante las infecciones bacterianas.
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