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Apoptosis of renal cortical cells in the hemolytic-uremic syndrome: : In vivo and in vitro studies

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Author

Summary, in English

This study examined apoptotic cell death associated with Shiga-like toxin (Stx)-producing Escherichia coli. Renal cortices from three children with postenteropathic hemolytic-uremic syndrome (HUS) and from mice infected with E. coli O157:H7 and pediatric renal tubular epithelial cells stimulated with Stx and E. coli O157:H7 extracts were examined for apoptotic changes. Apoptotic cells were detected by terminal dUTP nick end labeling of tubuli and glomeruli from HUS patients and from mice inoculated with Stx-2-positive and Stx-negative strains. Apoptosis was more extensive and severe ultramorphological nuclear and cytoplasmic changes were seen in the Stx-2-positive group. Stx caused DNA fragmentation and ultramorphological changes indicating apoptosis in cultured pediatric tubular cells. DNA fragmentation increased when cells were pre-stimulated with tumor necrosis factor alpha. Polymyxin extracts from Stx-2-positive and Stx-negative strains induced DNA fragmentation, but only extracts from Stx-2-positive strains caused ultramorphological changes and extensive DNA fragmentation. The results indicate that HUS is accompanied by increased apoptosis of kidney cells and that bacterial factors, possibly together with host cytokines in vivo, may activate apoptotic tissue injury.

Publishing year

1998-02

Language

English

Pages

636-644

Publication/Series

Infection and Immunity

Volume

66

Issue

2

Document type

Journal article

Publisher

American Society for Microbiology

Topic

  • Microbiology in the medical area

Keywords

  • Animals
  • Apoptosis
  • Bacterial Toxins
  • Child, Preschool
  • Female
  • Hemolytic-Uremic Syndrome
  • Humans
  • Infant
  • Kidney Cortex
  • Male
  • Mice
  • Mice, Inbred C3H
  • Microscopy, Electron
  • Polymyxins
  • Shiga Toxin 2
  • Tumor Necrosis Factor-alpha

Status

Published

Research group

  • Pediatric Nephrology

ISBN/ISSN/Other

  • ISSN: 0019-9567