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El desequilibrio de la microbiota inducido por el azúcar en la dieta interrumpe la protección mediada por el sistema
Yoshinaga Kawano1, Madeline Edwards1, Yiming Huang2
1Department of Microbiology and Immunology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Cell
|August 30, 2022
Resumen
Los microbios intestinales protegen contra el síndrome metabólico mediante la inducción de las células Th17. El azúcar en la dieta agota estos microbios protectores, aumentando el riesgo de enfermedad, pero la eliminación del azúcar restaura la protección.
Área de la Ciencia:
- Inmunología
- Microbiología
- Trastornos del metabolismo
Sus antecedentes:
- El papel de la microbiota intestinal en el síndrome metabólico no se comprende completamente.
- El síndrome metabólico, la obesidad y los fenotipos prediabéticos son preocupaciones de salud importantes.
- Las interacciones del sistema inmunológico con los microbios intestinales son cruciales para la salud metabólica.
Objetivo del estudio:
- Para investigar cómo los microbios intestinales regulan el síndrome metabólico.
- Identificar el papel de las células Th17 en la mediación de la protección contra la enfermedad metabólica.
- Para aclarar el impacto de la dieta, específicamente el azúcar, en la microbiota intestinal y las respuestas inmunes.
Principales métodos:
- Se utilizaron modelos de ratones alimentados con dietas altas en grasas y azúcar.
- Cambios analizados en la composición de la microbiota intestinal y las poblaciones de células Th17.
- Se investigó el papel de la IL-17 en la regulación de la absorción de lípidos.
- Se examinaron los efectos de la eliminación de azúcares en los parámetros metabólicos y la microbiota.
Principales resultados:
- La microbiota intestinal protege contra la obesidad y el síndrome metabólico mediante la inducción de células Th17 comensales específicas.
- Las dietas altas en grasa y azúcar agotan los microbios inductores de Th17, promoviendo enfermedades metabólicas.
- La restauración de las células Th17 revirtió el desarrollo de la enfermedad.
- La ingesta de azúcar media la pérdida de las células protectoras Th17, en parte a través de la proliferación de Faecalibaculum rodentium.
- La eliminación del azúcar de la dieta evitó el síndrome metabólico de una manera dependiente de Th17.
Conclusiones:
- Las células Th17 comensales específicas inducidas por la microbiota intestinal son críticas para prevenir el síndrome metabólico.
- El azúcar en la dieta interrumpe este mecanismo protector, contribuyendo a la patogénesis de la enfermedad metabólica.
- Las interacciones entre la dieta, la microbiota intestinal y la inmunidad intestinal son reguladores clave de la salud metabólica.
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