title: Expression of intrinsic factor in rat and murine gastric mucosal cell lineages is modified by inflammation.
abstract: 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 factor expression, two rodent models of chronic lymphocytic gastric inflammation were examined. Immunocytochemistry was performed using antiserum against human intrinsic factor and H/K ATPase (a parietal cell marker), counting the percent of intrinsic factor-positive parietal cells. HLA-B27 transgenic rats develop chronic gastritis at age 3 months. Congenic controls expressed intrinsic factor in 8.9 +/- 3.8% (mean +/- SD) of parietal cells; in inflamed areas of transgenic rats 21 +/- 5.2% (P < 0.0001) of parietal cells were positive. In adjacent areas without inflammatory infiltrate 16 +/- 3.6% of parietal cells contained intrinsic factor. C57BL/6 mice inoculated with Helicobacter felis develop gastritis by 4 weeks. After 4 and 8 weeks of infection, 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-1beta demonstrated a twofold increase in intrinsic factor-positive parietal cells. These 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 inflamed and adjacent noninflamed areas in the rat model suggest a tissue gradient of soluble inducer(s), possibly cytokines.
authors.affiliation: Division of Gastroenterology, Washington University School of Medicine, St. Louis, Missouri, USA.
authors.forename: J
authors.initials: J
authors.lastname: Shao
authors.forename: R B
authors.initials: RB
authors.lastname: Sartor
authors.forename: E
authors.initials: E
authors.lastname: Dial
authors.forename: L M
authors.initials: LM
authors.lastname: Lichtenberger
authors.forename: W
authors.initials: W
authors.lastname: Schepp
authors.forename: D H
authors.initials: DH
authors.lastname: Alpers
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified / Q000235:genetics; D002460:Cell Line; D002469:Cell Separation; D005260:Female; D005753:Gastric Mucosa / Q000166:cytology / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005756:Gastritis / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D015796:HLA-B27 Antigen / Q000235:genetics / Q000502:physiology; D016481:Helicobacter Infections; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000494:pharmacology; D007437:Intrinsic Factor / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D010295:Parietal Cells, Gastric / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew
chemical_list: D015796:HLA-B27 Antigen; D007375:Interleukin-1; D007437:Intrinsic Factor