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Los pili meningocócicos tipo IV reclutan el complejo de polaridad para cruzar el endotelio cerebral
Mathieu Coureuil1, Guillain Mikaty, Florence Miller
1Université Paris Descartes, Faculté de Médecine, INSERM (U-570), 75015 Paris, France. mathieu.coureuil@inserm.fr
Science (New York, N.Y.)
|June 13, 2009
Resumen
Neisseria meningitidis utiliza pili tipo IV para adherirse a las células cerebrales, reclutando el complejo Par3/Par6/PKCzeta. Esto interrumpe las uniones celulares, permitiendo a las bacterias romper la barrera hematoencefálica y causar meningitis.
Área de la Ciencia:
- Microbiología Microbiología.
- Biología celular Biología celular.
- La patogénesis y la patogénesis.
Sus antecedentes:
- Los pili tipo IV son cruciales para la adhesión del patógeno bacteriano a las células huésped.
- Neisseria meningitidis utiliza estos pili para adherirse a las células endoteliales del cerebro, lo que facilita el cruce de la barrera hematoencefálica (BBB).
- Comprender esta interacción es clave para prevenir la meningitis.
Objetivo del estudio:
- Para investigar los mecanismos moleculares de la adhesión de Neisseria meningitidis a las células endoteliales del cerebro humano.
- Para identificar los factores de la célula huésped reclutados por pili tipo IV durante la interacción bacteriana.
- Para aclarar cómo esta interacción facilita la penetración BBB.
Principales métodos:
- Co-cultivo de N. meningitidis con células endoteliales del cerebro humano.
- Microscopía de inmunofluorescencia para visualizar la localización de proteínas bacterianas y del huésped.
- Análisis del complejo de polaridad de la célula huésped y reclutamiento y distribución de proteínas de unión intercelular.
Principales resultados:
- La adhesión mediada por pili tipo IV de N. meningitidis recluta el complejo de polaridad Par3/Par6/PKCzeta a la interfaz bacteria-célula huésped.
- Este reclutamiento induce dominios de unión intercelular ectópicos en el sitio de interacción.
- Las proteínas de unión se agotan de las fronteras celular-célula, lo que lleva a la apertura de las uniones de las células endoteliales del cerebro.
Conclusiones:
- N. meningitidis explota la maquinaria de polaridad de la célula huésped a través de pili tipo IV para interrumpir las uniones de las células endoteliales.
- Este mecanismo facilita la translocación bacteriana a través de la barrera hematoencefálica.
- Dirigirse a esta interacción podría ofrecer nuevas estrategias terapéuticas contra la meningitis meningocócica.
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