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El equilibrio epitelial de IL-18 controla la función de barrera en la colitis

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|December 7, 2015
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Resumen
Este resumen es generado por máquina.

La interleucina-18 (IL-18) conduce a la colitis ulcerosa al interrumpir la barrera intestinal. El bloqueo de la señalización de IL-18 en las células epiteliales intestinales protege contra la colitis y preserva las células cápsulas.

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Área de la Ciencia:

  • Gastroenterología
  • Inmunología
  • Biología celular

Sus antecedentes:

  • La barrera de la mucosa intestinal, crucial para el control del microbioma, depende de las células de la copa que producen moco.
  • La función deteriorada de las células de la copa y la descomposición de la capa de moco son características de la enfermedad inflamatoria intestinal, específicamente la colitis ulcerosa.

Objetivo del estudio:

  • Investigar el papel de la interleucina-18 (IL-18) en el deterioro patológico de la integridad de la barrera intestinal durante la colitis.
  • Esclarecer el mecanismo por el cual la señalización de IL-18 en las células epiteliales intestinales influye en la maduración de las células de la copa y la gravedad de la colitis.

Principales métodos:

  • Utilizó un modelo de colitis en ratones.
  • Ratones genéticamente modificados generados con deleciones específicas de Il18, Il18r1 (receptor IL-18) en las células epiteliales intestinales, y Il18bp (proteína de unión a IL-18).
  • Se evaluó la gravedad de la colitis, el daño de la mucosa y la maduración de las células cápsulas mediante análisis histológicos y moleculares.

Principales resultados:

  • La eliminación de Il18 o Il18r1 en las células epiteliales intestinales confería una protección significativa contra la colitis y el daño de la mucosa.
  • La eliminación de Il18bp condujo a una colitis severa y a la pérdida de células cápsulas maduras.
  • La eliminación simultánea de Il18bp e Il18r1 en las células epiteliales intestinales rescató la colitis y la pérdida de células de copa, confirmando la señalización de IL-18 en las células epiteliales como el regulador clave.
  • Se encontró que la IL-18 inhibe la maduración de las células cálicas al alterar el programa de transcripción que rige el desarrollo de las células cálicas.

Conclusiones:

  • La señalización de IL-18 dentro de las células epiteliales intestinales es un factor crítico de la patología de la colitis y la disfunción de la barrera intestinal.
  • La orientación de la señalización de IL-18 en las células epiteliales intestinales representa una estrategia terapéutica potencial para la colitis ulcerosa.
  • La comprensión de la regulación de la IL-18 del desarrollo de las células cálicas es clave para abordar la disfunción de las células cálicas en la colitis ulcerosa.