Inflammatory bowel disease is a chronic inflammatory disease of the gut which manifests as ulcerative colitis or Crohn's disease. One of the most studied animal models of spontaneous Crohn's disease is the senescence-accelerated mouse (SAMP1/Yit strain) model. In SAMP1/Yit mice, although many immunological responses are perturbed, some evidence suggests that the primary defect lies in the epithelial cell barrier. In the process of studying epithelial permeability, we observed that the stomach in SAMP1/Yit mice also had increased permeability. Upon further examination, these mice were shown to have marked, chronic gastritis with focal to diffuse aggregates of mononuclear cells of mixed lineages. These aggregates were located predominantly in the oxyntic mucosa, with occasional lesions in the forestomach but with relatively fewer cellular infiltrates in the antral mucosa. Real-time RT PCR showed an increase in several helper T cell (Th cell)-derived pro-inflammatory cytokines in the gastric mucosa of SAMP1/Yit mice. However, many of the cells in the aggregates of SAMP1/Yit mice were B cells. SAMP1/Yit B cells exacerbate ileitis when co-transferred into immunodeficient recipients. The gastritis also reflects a contribution by B cells. As SAMP1/Yit mice were derived from AKR mice, we examined AKR mice and determined that they too have an increased occurrence of gastritis, although they do not develop ileitis. B cells contributed to the gastric inflammation in these mice also. Thus, SAMP1/Yit mice display gastritis as well as ileitis, and B cells appear to play a role in the pathogenesis of inflammation at both sites. This review will discuss some of the mechanisms that may account for these different manifestations of gastrointestinal disease.