Regulation of bactevial translocation by nitric oxide

Evan P. Nadler, Henri Ford

Research output: Contribution to journalShort survey

44 Citations (Scopus)

Abstract

Nitric oxide (NO) appears to play a paradoxical role in intestinal physiology. Although NO has potent bactericidal effects, a growing body of evidence suggests that it mediates intestinal injury and breakdown of gut barrier function. Data from our lab and others show an increased incidence of bacterial translocation following endotoxin challenge, and upregulation of inducible NO synthase (iNOS) mRNA and protein in the intestine. These phenomena co-localize with enterocyte apoptosis at the tips of the intestinal villi and immunoreactivity to nitrotyrosine. Electron microscopy reveals swollen mitochondria, implicating these organelles as putative targets for NO or its reactive nitrogen intermediates. We review some of the literature and discuss our current work in trying to define this mechanism.

Original languageEnglish (US)
Pages (from-to)165-168
Number of pages4
JournalPediatric Surgery International
Volume16
Issue number3
DOIs
StatePublished - Jan 1 2000
Externally publishedYes

Fingerprint

Nitric Oxide
Bacterial Translocation
Enterocytes
Nitric Oxide Synthase Type II
Endotoxins
Organelles
Intestines
Electron Microscopy
Mitochondria
Up-Regulation
Nitrogen
Apoptosis
Messenger RNA
Incidence
Wounds and Injuries
Proteins
3-nitrotyrosine

Keywords

  • Bacterial translocation
  • IgA
  • Inducible nitric oxide synthase
  • LPS
  • Nitric oxide

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Surgery

Cite this

Regulation of bactevial translocation by nitric oxide. / Nadler, Evan P.; Ford, Henri.

In: Pediatric Surgery International, Vol. 16, No. 3, 01.01.2000, p. 165-168.

Research output: Contribution to journalShort survey

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