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Variant form of diffuse corporal gastritis in NHE2 knockout mice
G P Boivin1, P J Schultheis, G E Shull
1Department of Pathology and Laboratory Medicine, University of Cincinnati School of Medicine, Ohio 45267-0529, USA.
Comparative Medicine
|December 1, 2000
Summary
Mice lacking the NHE2 gene develop early-onset gastritis, characterized by inflammation and parietal cell loss. This NHE2 null mutant mouse may serve as a model for studying prolonged achlorhydria effects.
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- The Na+/H+ exchanger 2 (NHE2) plays a role in gastric physiology.
- Gastritis is a common gastrointestinal disorder with various underlying causes.
Purpose of the Study:
- To investigate the long-term effects of NHE2 gene deficiency on gastric mucosa.
- To characterize the development and histological features of gastritis in NHE2 null mutant mice.
Main Methods:
- Histological examination of stomachs from NHE2 null mutant, heterozygous, and wild-type mice at various ages (10 days to 16 months).
- Assessment of cellular composition, hyperplasia, and presence of neoplasms.
Main Results:
- NHE2 null mutant mice developed gastritis with reduced parietal cells, transmural inflammation (neutrophils, lymphocytes, plasma cells), and hyperplasia of surface, enterochromaffin-like, and gastrin cells.
- Gastritis severity increased with age in mutant mice.
- No neoplasms were observed in mutant or control mice.
Conclusions:
- NHE2 deficiency leads to a unique form of early-onset gastritis distinct from autoimmune gastritis.
- The observed histological changes suggest prolonged achlorhydria as a contributing factor in adult NHE2-/- mice.
- NHE2 null mutant mice represent a valuable model for studying the consequences of chronic achlorhydria.
