Zusammenfassung
Dieses Symposium beschäftigte sich mit verschiedenen biologischen Manifestationen und Spätfolgen der Sepsis. Einige Teilnehmer haben versucht, Sepsis als ein rein chemisches Phänomen zu definieren, andere sind auf der Suche nach den sepsisgetriggerten Mediatoren, die die Gewebeschädigungen hervorrufen. Ein Mikrobiologe hingegen definiert Sepsis kurz als das Eindringen von Mikroorganismen und deren zelluläre Produkte (eingeschlossen sind Exo- und Endotoxine) in die Blutbahn und ihr dortiges Überleben. Hiernach resultiert die Sepsis aus dem Versagen eines oder mehrerer homöostatisch wirksamer Mechanismen, die Mikroben auf ihre symbiotischen Nischen wie Intestinum, obere Luftwege und Haut begrenzen oder eine Entfernung aus dem Blutkreislauf sichern. Bis die Mediatoren der Entzündung durch mikrobielle Produkte erfolgreich aktiviert worden sind und ihre Wirkung klinisch erkennbar ist, gestaltet sich eine Intervention schwierig, wenn nicht sogar unmöglich. Sepsis ist somit eine Frage der Interaktion zwischen dem Menschen und seiner mikrobiellen Flora, der immunologischen Effektormechanismen, die diese Interaktion steuern, und der früh und oft inapparent auftretenden pathologischen Ereignisse, die sie unterbrechen.
Diese Arbeit wurde durch die Stipendien AI 21620 und AI 21171 des United States Public Health Service und der Veterans Administration der USA unterstützt. Sie wurde von Frau May Fong maschinengeschrieben. Dies ist der Bericht Nr. 19 des Centre for Immunochemistry der University of California, San Francisco.
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Griffiss, J.M.L. (1989). Die Rolle der Antikörper bei bakterieller Sepsis. In: Reinhart, K., Eyrich, K. (eds) Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-09869-1_25
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