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La microbiota intestinal provoca una respuesta inmune protectora contra la transmisión de la malaria
Bahtiyar Yilmaz1, Silvia Portugal2, Tuan M Tran2
1Instituto Gulbenkian de Ciência, Rua da Quinta Grande, 6, 2780-156 Oeiras, Portugal.
Cell
|December 7, 2014
Resumen
La inactivación del gen UDP-galactosa:β-galactosida-α1-3-galactosiltransferasa (α1,3GT) protege contra la malaria. Los anticuerpos anti-α-gal generados por esta inactivación del gen se dirigen a los parásitos de Plasmodium, ofreciendo protección contra la infección.
Área de la Ciencia:
- Inmunología Inmunología.
- Biología evolutiva Biología evolutiva.
- Glucobiología Glucobiología.
Sus antecedentes:
- La glicosilación es crucial para la resistencia a las infecciones y está sujeta a la selección natural.
- El glicano Galα1-3Galβ1-4GlcNAc-R (α-gal) es expresado por patógenos como Plasmodium spp. y algunas bacterias.
- Los seres humanos suelen carecer de α-gal debido a la inactivación del gen UDP-galactosa:β-galactosida-α1-3-galactosiltransferasa (α1,3GT), lo que lleva a la producción de anticuerpos anti-α-gal.
Objetivo del estudio:
- Investigar si la ausencia de expresión de α-gal confiere protección contra la infección por Plasmodium.
- Determinar el papel de los anticuerpos anti-α-gal en la transmisión de la malaria y la defensa del huésped.
Principales métodos:
- Estudió la inactivación del gen α1,3GT y su efecto en la expresión de α-gal.
- Se analizó la presencia de α-gal en Plasmodium spp. y E. coli O86:B7.7. y también E. coli O86:B7.
- Se evaluó la asociación de anticuerpos anti-α-gal con la protección contra la malaria en humanos y ratones con deficiencia de α1,3GT.
- Investigó el mecanismo de eliminación de parásitos mediada por anticuerpos anti-α-gal.
- Vacunación evaluada contra el α-gal para la protección contra la malaria en un modelo de ratón.
Principales resultados:
- Ambos son Plasmodium spp. y también Plasmodium spp. y E. coli O86:B7 expresan el glicano α-gal.
- Los anticuerpos anti-α-gal están vinculados a la protección contra la transmisión de la malaria en humanos.
- Los ratones con deficiencia de α1,3GT, colonizados con E. coli O86:B7, produjeron anticuerpos protectores anti-α-gal.
- Los anticuerpos anti-α-gal inducen una citotoxicidad mediada por el complemento contra los esporozoitos de Plasmodium en la piel.
- La vacunación contra α-gal proporcionó protección estéril contra la malaria en ratones.
Conclusiones:
- La ausencia de expresión de α-gal y la presencia de anticuerpos anti-α-gal ofrecen protección contra la malaria.
- Los anticuerpos anti-α-gal neutralizan los parásitos Plasmodium inmediatamente después de la inoculación del mosquito.
- Dirigirse al glicano α-gal a través de la vacunación presenta una estrategia potencial para reducir la transmisión de la malaria en humanos.
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