Chronic Atrophic Gastritis in SCID Mice Experimentally Infected withCampylobacter fetus

Abstract

Campylobacter fetusis a cause of enteritis and invasive extraintestinal disease in humans. In order to develop an animal model ofC. fetusinfection, outbred ICR SCID mice were orally challenged with a clinical isolate ofC. fetus. The stomachs of SCID mice were heavily colonized withC. fetus, and colonization was associated with the development of chronic atrophic gastritis. This lesion was characterized by an inflammatory infiltrate of granulocytes and macrophages that over time resulted in a loss of specialized parietal and chief cells in the corpus and the appearance of a metaplastic mucous epithelium. This lesion bears similarity to that encountered during experimental murine infection withHelicobacter pyloriorHelicobacter felis. Despite colonization of the cecum and colon tissues byC. fetusin SCID mice, no lesions were noted in these tissues. A follow-up study confirmed these findings for SCID mice and also demonstrated thatC. fetuscould also infect the gastric mucosa of wild-type, outbred ICR mice. However, in ICR mice, the anatomic extent of colonization was more limited and the severity of inflammation and epithelial alterations was significantly less than that observed in infected SCID mice. The stomach may represent an unrecognized environmental niche forCampylobacterspecies.