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La interacción siderocalina / enterobactina: un vínculo entre la inmunidad de los mamíferos y el transporte de hierro

Rebecca J Abergel¹, Matthew C Clifton, Juan C Pizarro

¹Department of Chemistry, University of California, Berkeley, California 94720-1460, USA.

Journal of the American Chemical Society

|August 6, 2008

Resumen

La siderocalina (Scn) secuestra los complejos bacterianos de enterobactina (Ent) y hierro. Las condiciones ácidas causan la liberación de hierro mediante la degradación de Ent y la alteración de su coordinación, lo que afecta a Scnn.

Área de la Ciencia:

Microbiología Microbiología.
La bioquímica es la bioquímica.
Inmunología Inmunología.

Sus antecedentes:

La enterobactina (Ent) es un sideróforo para la captación de hierro en las bacterias entéricas.
La siderocalina (Scn) es una proteína inmune que secuestra los complejos de ent-hierro, actuando como un agente antibacteriano.
Se está investigando el papel del Scn en el transporte de hierro y la depuración de sideróforos, en particular su mecanismo en ambientes ácidos.

Objetivo del estudio:

Para investigar la interacción entre la enterobactina férrica ([Fe ((III)) ((Ent)) ((3-)) y la siderocalina (Scn) a diferentes niveles de pH.
Comprender la dinámica estructural y de unión de los mutantes de Scn con [Fe (III) (Ent) ] (III-).
Para dilucidar el mecanismo de liberación de hierro de los sideróforos ligados al Scn bajo condiciones ácidas.

Principales métodos:

Preparación y análisis estructural de proteínas Scn mutantes (Scn-W79A/R81A y Scn-Y106F).
Estudios vinculantes utilizando espectroscopias de fluorescencia, UV-vis y EXAFS.
Análisis dependiente del pH de las constantes de disociación Scn/sideróforo y coordinación del hierro.

Principales resultados:

Las proteínas Scn mutantes mostraron una afinidad reducida por [Fe (III) (Ent) [3-) sin alterar la conformación general de la proteína.
La unión de Scn inhibe el cambio de coordinación dependiente del pH de Ent de catecolato a salicilato.
La acidificación fuerte conduce a la liberación de hierro y la degradación de Ent, con evidencia de que ambos mecanismos contribuyen a la liberación de hierro.

Conclusiones:

La liberación de hierro de la enterobactina ligada al Scn en endosomas ácidos es probablemente mediada por una combinación de degradación de Ent y coordinación alterada del hierro.
Comprender este mecanismo es crucial dado el papel potencial de Scn en el transporte celular del hierro.
Los estudios de mutagenesis proporcionan información sobre la base estructural de las interacciones Scn-siderophore.

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