Abstract

The relationship between gastric inflammation caused by Helicobacter pylori infection and symptoms of dyspepsia remains controversial (1). Using a murine model of gastric infection, Bercik et al provide new insights into the mechanism underlying such interactions. Gastric sections from Balb/c mice infected with H pylori, strain SS-1, were used for both histological evaluation and studies of neuromuscular physiology. Acute infection (two weeks) caused an antral-predominant polymorphonuclear cell infiltrate that was superceded by a corpus-predominant mononuclear and macrophage infiltrate in chronic infection (three to 16 months).