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Un patógeno bacteriano extracelular modula el metabolismo del huésped para regular su propia detección y
Moshe Baruch1, Ilia Belotserkovsky1, Baruch B Hertzog1
1Department of Microbiology and Molecular Genetics, The Hebrew University of Jerusalem, Faculty of Medicine, Jerusalem 91120, Israel.
Cell
|January 21, 2014
Resumen
La infección por estreptococos del grupo A (GAS) se basa en la adquisición de nutrientes. Las bacterias detectan la asparagina liberada por el huésped (ASN), alterando la expresión génica y la virulencia, ofreciendo un objetivo terapéutico.
Área de la Ciencia:
- Microbiología Microbiología.
- Enfermedades infecciosas Enfermedades infecciosas.
- Biología Molecular Biología Molecular
Sus antecedentes:
- El estreptococo del grupo A (GAS) es un patógeno humano significativo.
- La adquisición de nutrientes es crucial para la supervivencia bacteriana y la progresión de la infección.
- Comprender las interacciones entre GAS y el huésped es vital para desarrollar tratamientos efectivos.
Objetivo del estudio:
- Para aclarar el papel de la asparagina (ASN) en la patogénesis de GAS.
- Para identificar los factores de virulencia GAS regulados por ASN.
- Explorar el metabolismo de la ASN como un objetivo terapéutico potencial contra las infecciones por GAS.
Principales métodos:
- Utilizó el sistema sil de detección de quórum como reportero en GAS.
- Investigó la interacción de GAS con las células huésped y la entrega de toxinas.
- Los cambios en la expresión génica analizados en respuesta a ASN.
- Evaluó el impacto de la asparaginasa en el crecimiento de GAS in vitro e in vivo.
Principales resultados:
- El GAS libera las toxinas de la estreptolisina, induciendo estrés en el retículo endoplasmático en las células huésped.
- El estrés de la célula huésped eleva la producción de ASN, que GAS detecta.
- La ASN influye en la expresión de aproximadamente el 17% de los genes GAS, incluida la regulación al alza de las toxinas estreptolisinas y la regulación a la baja de los genes de proliferación.
- La asparaginasa inhibe eficazmente el crecimiento de GAS en la sangre humana y en un modelo de bacteriemia de ratón.
Conclusiones:
- GAS emplea un mecanismo sofisticado para adquirir nutrientes mediante la manipulación de las respuestas al estrés de las células huésped.
- ASN actúa como una molécula de señalización clave en GAS, regulando la expresión del factor de virulencia.
- Dirigirse al metabolismo de la ASN con asparaginasa presenta una estrategia terapéutica prometedora contra las infecciones por GAS.
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