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

Karpman, D LU ; Håkansson, Anders P LU ; Perez, M T LU ; Isaksson, C LU ; Carlemalm, E LU ; Caprioli, A and Svanborg, C LU (1998) In Infection and Immunity 66(2). p.636-644
Abstract

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... (More)

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.

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organization
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Contribution to journal
publication status
published
subject
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
in
Infection and Immunity
volume
66
issue
2
pages
9 pages
publisher
American Society for Microbiology
external identifiers
  • Scopus:2642704194
ISSN
0019-9567
language
English
LU publication?
yes
id
2bddece6-79f7-4e39-a295-ea494989de7c
date added to LUP
2016-05-21 11:36:20
date last changed
2016-10-13 05:09:15
@misc{2bddece6-79f7-4e39-a295-ea494989de7c,
  abstract     = {<p>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.</p>},
  author       = {Karpman, D and Håkansson, Anders P and Perez, M T and Isaksson, C and Carlemalm, E and Caprioli, A and Svanborg, C},
  issn         = {0019-9567},
  keyword      = {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},
  language     = {eng},
  number       = {2},
  pages        = {636--644},
  publisher    = {ARRAY(0xacc3708)},
  series       = {Infection and Immunity},
  title        = {Apoptosis of renal cortical cells in the hemolytic-uremic syndrome: : In vivo and in vitro studies},
  volume       = {66},
  year         = {1998},
}