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Molekularer Mechanismus von Clostridium difficile Toxin A und B

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Ökosystem Darm VII
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Zusammenfassung

Ungefähr 20% der sog. „Antibiotika-assoziierten“ Diarrhöen werden mit Clostridium difficile in Zusammenhang gebracht. Weit größer ist die Bedeutung dieses Keims für die durch Antibiotika induzierte Kolitis. Es wird angenommen, daß in über 90% der Fälle einer pseudomembranösen Kolitis, die als Folge einer Antibiotikatherapie auftritt, C. difficile der entscheidende Keim ist [1–6]. Als wesentliche Pathogenitätsfaktoren von C. difficile werden die Toxine A und B angesehen. Toxin A, das im Tiermodell Diarrhö, Entzündung und Nekrose der Darmschleimhaut verursacht, wird auch als Enterotoxin bezeichnet. Dagegen zeigt das Toxin B unter gleichen Bedingungen keine Enterotoxizität [7, 8]. Diese Unterschiede in den Wirkungen der Toxine sind vermutlich auf unterschiedliche Zellrezeptoren für Toxin A und B zurückzuführen. Leider sind die Toxinrezeptoren der eukaryonten Zielzellen noch unbekannt. Es wird vermutet, daß es sich dabei um Glycoproteine handelt. Wesentliche Fortschritte in der Erforschung der C. difficile Toxine konnten kürzlich durch die Klonierung und Sequenzierung der Gene von C. difficile Toxin A und B erreicht werden [9–14]. Danach bestehen C. difficile Toxin A und B aus 2710 bzw. 2366 Aminosäuren, haben ein Molekulargewicht von ~308 bzw. 270 kDa und sind in ihrer Aminosäuresequenz untereinander ~49% identisch und ~63% homolog.

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Aktories, K. (1996). Molekularer Mechanismus von Clostridium difficile Toxin A und B. In: Kist, M., Caspary, W.F., Lentze, M.J. (eds) Ökosystem Darm VII. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-80327-7_8

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  • DOI: https://doi.org/10.1007/978-3-642-80327-7_8

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-540-61817-1

  • Online ISBN: 978-3-642-80327-7

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