Expression of intrinsic factor in rat and murine gastric mucosal cell lineages is modified by inflammation

Intrinsic factor is produced primarily by chief cells in rat and mouse, but 4 to 11% of isolated rat parietal cells also contain intrinsic factor. To test whether local conditions could alter the distribution of intrinsic fac tor expression, two rodent models of chronic lymphocytic gastric inflammati on were examined. Immunocytochemistry was performed using antiserum against human intrinsic factor and H/K ATPase (a parietal cell marker), counting t he percent of intrinsic factor-positive parietal cells. HLA-B27 transgenic rats develop chronic gastritis at age 3 months. Congenic controls expressed intrinsic fatter in 8.9 +/- 3.8% (mean +/- SD) of parietal cells; in infla med areas of transgenic rats 21 +/- 5.2% (P < 0.0001) of parietal cells wer e positive. In adjacent areas without inflammatory infiltrate 16 +/- 3.6% o f parietal cells contained intrinsic factor. C57BL/6 mice inoculated with H elicobacter felis develop gastritis by 4 weeks. After 4 and 8 weeks of infe ction, intrinsic factor-positive parietal cells increased from 7.8 +/- 2.8% in the congenic controls to 17.6 +/- 4.1% in the inflamed gastric body (P < 0.0001). Isolated rat parietal cells incubated with interleukin-lp demons trated a twofold increase in intrinsic factor-positive parietal cells. Thes e studies are consistent with the concept that intrinsic factor expression is both predetermined in chief cells and can be expressed in parietal cells in response to local inflammatory factors. The differences between inflame d and adjacent noninflamed areas in the rat model suggest a tissue gradient of soluble inducer(s), possibly cytokines.