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Helicobacter pylori SabA se adhiere en la infección persistente y la inflamación crónica
Jafar Mahdavi1, Berit Sondén, Marina Hurtig
1Department of Odontology/Oral Microbiology, Umeå University, SE-901 87 Umeå, Sweden.
Science (New York, N.Y.)
|July 27, 2002
Resumen
Helicobacter pylori utiliza los sialyl-Lewis x glicosfingolipidos como receptores en el estómago. Esta unión, mediada por la adhesina que se une al ácido siálico (SabA), contribuye a la virulencia de la bacteria y a la infección crónica.
Área de la Ciencia:
- Microbiología Microbiología.
- Inmunología Inmunología.
- Glucobiología Glucobiología.
Sus antecedentes:
- La infección por Helicobacter pylori (H. pylori) es una de las principales causas de gastritis y úlceras pépticas.
- La adherencia bacteriana a la mucosa gástrica es crucial para la colonización y virulencia de H. pylori.
- Las adhesinas específicas y los receptores del huésped median la unión de H. pylori.
Objetivo del estudio:
- Para identificar el receptor huésped específico para la adherencia de H. pylori.
- Para caracterizar la adhesión bacteriana involucrada en la unión a este receptor.
- Para investigar el papel de esta interacción en la infección por H. pylori y la virulencia.
Principales métodos:
- Identificación del sialyl-dimeric-Lewis x glicosfingolipido como el receptor de H. pylori.
- Aislamiento de la adhesina que se une al ácido siálico (SabA) mediante el método de "reetiquetado".
- Identificación del gen sabA (JHP662 / HP0725). identificación del gen sabA (JHP662 / HP0725). identificación del gen sabA (JHP662 / HP0725). identificación del gen sabA (JHP662 / HP0725).
- Demostración de la formación inducida del antígeno sialyl-Lewis x durante la infección por H. pylori in vivo.
Principales resultados:
- Sialyl-dimeric-Lewis x glycosphingolipid fue identificado como un receptor huésped clave para H. pylori.
- La infección por H. pylori indujo la formación de antígenos sialyl-Lewis x en el epitelio gástrico en humanos y monos rhesus.
- Se identificó la adhesina de unión al ácido siálico (SabA) y su gen sabA correspondiente.
Conclusiones:
- La interacción entre H. pylori y los antígenos sialyl-Lewis x, mediada por SabA, es un factor significativo en la patogénesis de H. pylori.
- Este mecanismo de adherencia probablemente contribuye a la capacidad de la bacteria para establecer infecciones crónicas.
- Dirigirse a esta interacción adhesina-receptor puede ofrecer nuevas estrategias terapéuticas contra H. pylori.
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