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Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

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Una familia de factores de virulencia bacteriana conservados amortigua las respuestas al interferón al bloquear la

Noémie Alphonse¹, Joseph J Wanford², Andrew A Voak²

¹Department of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London, UK; Immunoregulation Laboratory, Francis Crick Institute, London, UK.

|May 14, 2022

Resumen

Las bacterias Shigella bloquean la señalización del interferón (IFN) al dirigirse a la calmodulina, un sensor clave del calcio. Este mecanismo, que involucra a las proteínas OspC, impide la respuesta inmune y se conserva en otros patógenos.

Área de la Ciencia:

Microbiología
Inmunología
Biología molecular

Sus antecedentes:

Los interferones (IFN) son cruciales para la inmunidad antiviral y antibacteriana.
La evasión bacteriana de las respuestas IFN es una estrategia de virulencia significativa, pero los mecanismos siguen siendo poco conocidos.

Objetivo del estudio:

Para investigar si los patógenos bacterianos, específicamente Shigella, pueden evadir la señalización del interferón.
Elucidar los mecanismos moleculares por los cuales Shigella inhibe las respuestas IFN.

Principales métodos:

Investigó el papel de los efectores Shigella OspC en el bloqueo de la señalización IFN.
Se utilizaron ensayos bioquímicos para demostrar la unión de OspC1 y OspC3 a la calmodulina (CaM).
Se evaluó el crecimiento bacteriano en células epiteliales y un modelo de infección murina, con y sin agotamiento del receptor IFN.

Principales resultados:

Los efectores de Shigella OspC inhiben la señalización de IFN independientemente de la inhibición de la muerte celular.
OspC1 y OspC3 se unen a CaM, bloqueando las vías de señalización de CaM quinasa II y JAK/STAT.
Shigella que carece de OspC1 y OspC3 mostró un crecimiento atenuado, que fue rescatado por el agotamiento de los receptores IFN.
Los homólogos de OspC conservados en otros patógenos también se unen a CaM e inhiben la señalización de IFN.

Conclusiones:

Shigella emplea un nuevo mecanismo para inhibir las respuestas IFN al apuntar a la CaM y a la señalización posterior.
La evasión de IFN a través del antagonismo de CaM es una estrategia de virulencia conservada entre los patógenos bacterianos.
Este estudio destaca la importancia de la señalización de Ca2+ y la orientación de IFN en la patogénesis bacteriana.

Palabras clave:

Ca ((2+)Se trata de la siguiente:Las ISG JAK y STAT En el caso de los En el caso de los La Shigella T3SS (en inglés)el calcio Calmodulina y sus derivados Interacciones huésped-patógeno Interferones y sus derivados

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