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La proteína M1 del estreptococo construye una red de fibrinógeno de huésped patológico.

Pauline Macheboeuf¹, Cosmo Buffalo, Chi-yu Fu

¹Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, California 92093, USA.

|April 9, 2011

Resumen

La proteína Streptococcus M1 forma un complejo único con fibrinógeno, activando los neutrófilos y causando síntomas similares al choque tóxico. Comprender esta estructura revela cómo las bacterias causan lesiones graves en los tejidos.

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Área de la Ciencia:

Microbiología Microbiología.
Biología Estructural Biología estructural.
Inmunología Inmunología.

Sus antecedentes:

El estreptococo del grupo A (GAS) es una de las principales causas de infecciones invasivas.
La proteína M1 es un importante factor de virulencia GAS responsable de los síntomas similares al shock tóxico.
La activación de los neutrófilos es crítica en la patogénesis del shock tóxico estreptocócico.

Objetivo del estudio:

Proporcionar una explicación estructural de las propiedades patológicas del complejo M1-fibrinógeno.
Para dilucidar el mecanismo de activación de neutrófilos inducida por M1.
Comprender las bases estructurales del shock tóxico estreptocócico.

Principales métodos:

Cristalografía de rayos X para determinar la estructura del complejo M1-fibrinógeno.
Pruebas bioquímicas para evaluar la activación de los neutrófilos.
Análisis de la formación de la red supramolecular.

Principales resultados:

El dímero de proteína M1 organiza cuatro moléculas de fibrinógeno en un patrón parecido a una cruz.
Esta red supramolecular específica es esencial para la activación de los neutrófilos.
La interrupción de esta red evita resultados patológicos.
La red es distinta de un típico coágulo de fibrina.

Conclusiones:

La estructura única del complejo M1-fibrinógeno explica su papel en la inducción de fugas vasculares y lesiones tisulares.
La activación de los neutrófilos está mediada por una red supramolecular específica formada por el complejo.
Estos hallazgos ofrecen información sobre la fisiopatología del shock tóxico estreptocócico.