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Los esfingolipidos de un microbio simbiótico regulan la homeostasis de las células T asesinas naturales intestinales
Dingding An1, Sungwhan F Oh1, Torsten Olszak2
1Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Cell
|January 21, 2014
Resumen
El microbio intestinal Bacteroides fragilis utiliza esfingolípidos únicos para limitar la proliferación de células T (iNKT) asesinas naturales invariantes, protegiendo contra la colitis. Esta modulación inmune temprana ofrece un potencial terapéutico para las enfermedades autoinmunes y alérgicas.
Área de la Ciencia:
- Microbiología Microbiología.
- Inmunología Inmunología.
- Gastroenterología y Gastroenterología.
Sus antecedentes:
- La fisiología de los mamíferos está formada por la coevolución con los microbios intestinales.
- Las células T asesinas naturales invariables (iNKT) juegan un papel crucial en la homeostasis inmune.
Objetivo del estudio:
- Para investigar cómo Bacteroides fragilis influye en la homeostasis de las células iNKT.
- Para determinar el potencial terapéutico de los esfingolipidos bacterianos en la modulación de las respuestas de las células iNKT.
Principales métodos:
- Estudió ratones neonatales que carecían de esfingolipidos bacterianos.
- Se han administrado glycosphingolipids de B. fragilis, incluyendo GSL-Bf717, a ratones.
- Se evaluó el número de células iNKT y la protección contra la colitis inducida por oxazolona.
Principales resultados:
- Bacteroides fragilis complementa los lípidos del huésped con esfingolípidos inhibidores, impidiendo la proliferación celular iNKT.
- La exposición neonatal a los esfingolipidos bacterianos restringe el número de células iNKT en la edad adulta.
- El tratamiento con GSL-Bf717 redujo el número de células iNKT y protegió contra la colitis.
Conclusiones:
- Los esfingolipidos bacterianos, como GSL-Bf717, inhiben el desarrollo y la función de las células iNKT.
- Estas moléculas ofrecen una estrategia terapéutica potencial para los trastornos autoinmunes y alérgicos mediados por células iNKT.
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