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TLR13 reconoce el ARNr 23S bacteriano desprovisto de la modificación que forma la resistencia a la eritromicina

Marina Oldenburg¹, Anne Krüger, Ruth Ferstl

¹Institute of Medical Microbiology, University of Duisburg-Essen, Essen, Germany.

Science (New York, N.Y.)

|July 24, 2012

Resumen

Los ratones poseen un receptor de tipo Toll 13 (TLR13) que reconoce el ARN ribosomal bacteriano 23S (ARNr), el objetivo de los antibióticos MLS. Los mecanismos de resistencia a los antibióticos en las bacterias pueden evadir este reconocimiento inmune crucial.

Área de la Ciencia:

Inmunología Inmunología.
Microbiología Microbiología.
Biología Molecular Biología Molecular

Sus antecedentes:

La inmunidad innata depende de los receptores de reconocimiento de patrones (PRR) como los receptores Toll-like (TLR) para detectar patógenos.
El receptor tipo peaje 13 (TLR13) es un receptor huérfano con un ligando natural desconocido.

Objetivo del estudio:

Para identificar el ligando natural para el receptor de tipo Toll 13 (TLR13) del ratón.
Investigar el papel de TLR13 en el reconocimiento de componentes bacterianos y su evasión por los mecanismos de resistencia a los antibióticos.

Principales métodos:

Los ensayos de estimulación utilizan oligoribonucleótidos sintéticos y el ARN ribosomal 23S bacteriano (ARNr).
Prueba de la respuesta de TLR13 al ARNr de cepas bacterianas resistentes a los antibióticos.
Análisis de la activación de TLR13 por el ARNr modificado que imita la resistencia a los antibióticos.

Principales resultados:

TLR13 reconoce una secuencia específica conservada dentro del ARN ribosomal 23S (ARNr) bacteriano.
Esta secuencia de ARNr 23S es el sitio de unión para los antibióticos macrolide, lincosamida y estreptogramina (MLS).
El ARNr de Staphylococcus aureus 23S resistente a la eritromicina y el ARNr modificado no pudieron activar el TLR13, lo que indica una evasión inmune.

Conclusiones:

El ARNr 23S bacteriano es un ligando natural para el ratón TLR13.
Los mecanismos de resistencia a los antibióticos bacterianos, específicamente las modificaciones en el ARNr 23S, sirven como una estrategia para evadir la detección inmune del huésped a través de TLR13.

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