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The Role of Piglet Intestinal Mucus in the Pathogenicity of Escherichia coli K88

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Molecular Pathogenesis of Gastrointestinal Infections

Part of the book series: Federation of European Microbiological Societies Symposium Series ((FEMS,volume 58))

Summary

The influence of mucus overlying the epithelial cells in the piglet ileum, on the colonization potential of enterotoxigenic E. coli K88 fimbriated cells was investigated. Using in vitro assays, colonization potential was assessed in terms of growth in mucus, presence of K88 receptors in mucus as well as penetration capacity of K88 fimbriated cells through mucus and subsequently adhesion to underlying epithelial cells. As piglet susceptibility to K88 strains is age related, ileal mucosa were sampled from piglets 0–45 days old. E. coli K88 cells grew well in mucus from all ages tested, however, the amount of K88 fimbrial receptor varied significantly with age, with almost undetectable levels in the newborn. The K88 specific mucus receptor could be removed by ultra centrifuging and therefore must be located on a large molecular weight component or fragment. Although the amount of receptor in the mucus had no effect on penetration of K88 bearing cells through the mucus, E. coli K88 cells could not adhere to epithelial cells after passage through receptor-rich mucus. Receptor-poor mucus had no effect on such adhesion. In considering the role of mucus in the pathogenicity mechanism, the questions can be posed: Will the mucus be a site of colonization? Can the presence of mucus receptor protect the piglet from disease?

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© 1991 Plenum Press, New York

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Conway, P.L., Blomberg, L., Welin, A., Cohen, P.S. (1991). The Role of Piglet Intestinal Mucus in the Pathogenicity of Escherichia coli K88. In: Wadström, T., Mäkelä, P.H., Svennerholm, AM., Wolf-Watz, H. (eds) Molecular Pathogenesis of Gastrointestinal Infections. Federation of European Microbiological Societies Symposium Series, vol 58. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5982-1_48

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  • DOI: https://doi.org/10.1007/978-1-4684-5982-1_48

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-5984-5

  • Online ISBN: 978-1-4684-5982-1

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