Epithelial attachment alters the outcome of <i>Helicobacter pylori</i> infection

DOI Web Site 被引用文献8件
  • Janaki L. Guruge
    Departments of Molecular Biology and Pharmacology, Pathology and Medicine, and Molecular Microbiology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St. Louis, MO 63110; Department of Medicine, Karolinska Institute, Stockholm, Sweden; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232
  • Per G. Falk
    Departments of Molecular Biology and Pharmacology, Pathology and Medicine, and Molecular Microbiology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St. Louis, MO 63110; Department of Medicine, Karolinska Institute, Stockholm, Sweden; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232
  • Robin G. Lorenz
    Departments of Molecular Biology and Pharmacology, Pathology and Medicine, and Molecular Microbiology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St. Louis, MO 63110; Department of Medicine, Karolinska Institute, Stockholm, Sweden; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232
  • Maria Dans
    Departments of Molecular Biology and Pharmacology, Pathology and Medicine, and Molecular Microbiology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St. Louis, MO 63110; Department of Medicine, Karolinska Institute, Stockholm, Sweden; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232
  • Hans-Peter Wirth
    Departments of Molecular Biology and Pharmacology, Pathology and Medicine, and Molecular Microbiology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St. Louis, MO 63110; Department of Medicine, Karolinska Institute, Stockholm, Sweden; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232
  • Martin J. Blaser
    Departments of Molecular Biology and Pharmacology, Pathology and Medicine, and Molecular Microbiology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St. Louis, MO 63110; Department of Medicine, Karolinska Institute, Stockholm, Sweden; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232
  • Douglas E. Berg
    Departments of Molecular Biology and Pharmacology, Pathology and Medicine, and Molecular Microbiology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St. Louis, MO 63110; Department of Medicine, Karolinska Institute, Stockholm, Sweden; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232
  • Jeffrey I. Gordon
    Departments of Molecular Biology and Pharmacology, Pathology and Medicine, and Molecular Microbiology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St. Louis, MO 63110; Department of Medicine, Karolinska Institute, Stockholm, Sweden; and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232

書誌事項

公開日
1998-03-31
DOI
  • 10.1073/pnas.95.7.3925
公開者
Proceedings of the National Academy of Sciences

この論文をさがす

説明

<jats:p> Genetically defined <jats:italic>in vivo</jats:italic> models are needed to assess the importance of target cell attachment in bacterial pathogenesis. Gastric colonization by <jats:italic>Helicobacter pylori</jats:italic> in human populations is common and persistent, and has various outcomes including peptic ulcers and cancer. The impact of attachment on the course of infection was examined in transgenic mice expressing a human receptor for <jats:italic>H. pylori</jats:italic> in their gastric epithelium. Persistent infection by a clinical isolate occurred at comparable microbial densities in transgenic and nontransgenic littermates. However, microbial attachment in transgenic mice resulted in production of autoantibodies to Lewis <jats:sup>x</jats:sup> carbohydrate epitopes shared by bacteria and acid-secreting parietal cells, chronic gastritis, and parietal cell loss. This model should help identify bacterial and host genes that produce attachment-related pathology. </jats:p>

収録刊行物

被引用文献 (8)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ