Gastritis associated with infection by Helicobacter pylori: comparative pathology in humans and swine

Infection of humans with Helicobacter pylori elicits a multifocal, active, chronic inflammatory response and moderate to severe atrophy of the gastric mucosa. Currently, piglets are the only reported animal model of H. pylori infection. Our objective was to compare the inflammatory response induced in humans with that induced in piglets by H. pylori infection. Samples of gastric mucosa were obtained from H. pylori-infected and uninfected piglets and humans. The composition of the inflammatory cell infiltrate and mucosal atrophy were evaluated by histomorphometric analysis of the biopsied gastric tissue. Infection with H. pylori resulted in a three-fold increase in the volume of inflammatory cells in the gastric mucosa of both humans and piglets. In H. pylori-infected humans, neutrophils composed the bulk of the cellular infiltrate; in piglets, the primary inflammatory cell was the lymphocyte. Both humans and piglets had severe epithelial cell vacuolation and significant reduction of the gastric mucosal surface area. We concluded that pathologic processes induced by infection with H. pylori, which include relatively severe mucosal inflammation, mucosal atrophy, and epithelial vacuolation, are similar in piglets and humans but that the primary inflammatory cell types are distinctly different in the two species.