Neutrophil-mediated injury to gastric mucosal surface cells

R. Kozol, A. Kopatsis, S. E.G. Fligiel, R. Czanko, D. Callewaert

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Neutrophils (PMNs) have been implicated in the pathogenesis of gastritis. This study evaluates the magnitude and mode of PMN-mediated damage to gastric mucosal surface cells (GSC) in a system independent of vascular and neural factors. Rabbit GSC were freshly isolated and preloaded with51Cr. GSC were then incubated for 1 hr or 4 hr with freshly isolated human PMNs at varying effector-to-target cell ratios. Injury to GSC was assessed as percent specific51Cr released and by electron microscopy. We found minimal GSC injury using nonactivated PMNs. Incubation with PMNs activated with formylmethionyl-leucyl-phenalalanine (FMLP), however, resulted in significant GSC injury at the 20:1 PMN/GSC ratio, 33.2±1.8%51Cr release (P<0.001 compared to nonactivated PMNs). Electron microscopy revealed well-preserved gastric surface cells after exposure to nonstimulated PMNs. GSC exposed to activated PMNs (20:1 PMN/GSC ratio) were severely injured. Proteinase inhibitors and dimethylsulfoxide failed to diminish PMN-mediated GSC injury. Conversely, superoxide dismutase (SOD) inhibited GSC injury by more than 50% (P<0.001). In addition, glutathione peroxidase inhibited injury by 84% (P<0.001). These data suggest that neutrophil-mediated injury to gastric surface cells in vitro involves superoxide anion and hypochlorous acid and not neutral trypsinlike proteinases or hydroxyl radicals.

Original languageEnglish (US)
Pages (from-to)138-144
Number of pages7
JournalDigestive Diseases and Sciences
Issue number1
StatePublished - Jan 1 1994


  • free radicals
  • gastric mucosa
  • gastric mucosal injury
  • gastritis
  • neutrophils

ASJC Scopus subject areas

  • Gastroenterology


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