Evaluation of Lineage Changes in the Gastric Mucosa Following Infection With and Specified Intestinal Flora in INS-GAS Mice.

Pinzon-Guzman C, Meyer AR, Wise R, Choi E, Muthupalani S, Wang TC, Fox JG, Goldenring JR
J Histochem Cytochem. 2019 67 (1): 53-63

PMID: 29969055 · PMCID: PMC6309034 · DOI:10.1369/0022155418785621

Gastric adenocarcinoma develops in metaplastic mucosa associated with infection in the stomach. We have sought to evaluate the precise lineage changes in the stomachs of insulin-gastrin (INS-GAS) mice infected with and/or intestinal flora (Altered Schaedler's Flora; ASF). Stomachs from groups infected with contained progressive spasmolytic polypeptide-expressing metaplasia (SPEM) compared with germ-free and mice infected with ASF alone. The overall phenotype of the -infected mice was dominated by Ulex europaeus lectin (UEAI)-positive foveolar hyperplasia that was distinct from GSII/CD44v9-positive SPEM. However, in the mice with co-infected with ASF, we identified a subpopulation of UEAI-positive foveolar cells that co-expressed intestinal mucin 4 (MUC4). These regions of foveolar cells were variably positive for CD44v9 as well as TFF3. Interestingly, an intravascular lesion identified in a dual /ASF-infected mouse expressed both UEAI and . Finally, we identified an increase in the number of tuft cells within the mucosa of -infected groups. Our findings suggest that infection promotes foveolar hyperplasia as well as metaplasia, while co-infection may promote progressive foveolar and metaplastic lesions as well as dysplasia. Grading of gastric lesions in mice as preneoplastic requires multiple immunostaining markers to assign lineage derivation and behavior.

MeSH Terms (14)

Adenocarcinoma Animals Gastric Mucosa Gastrointestinal Microbiome Helicobacter Infections Helicobacter pylori Hyaluronan Receptors Immunohistochemistry Intercellular Signaling Peptides and Proteins Male Mice Mucin-4 Protein-Serine-Threonine Kinases Stomach Neoplasms

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