Evaluation of Lineage Changes in the Gastric Mucosa Following Infection With Helicobacter pylori and Specified Intestinal Flora in INS-GAS Mice. (January 2019)

• Record Type: Journal Article
• Authors: Pinzon-Guzman, Carolina; Meyer, Anne R.; Wise, Rachel; Choi, Eunyoung; Muthupalani, Sureshkumar; Wang, Timothy C.; Fox, James G.; Goldenring, James R.
• Is Part Of: Journal of histochemistry and cytochemistry. Volume 67:Number 1(2019:Jan.)
• Page Start: 53
• Page End: 63
• Publication Date: 2019-01
• Subjects: carcinogenesis -- CD44 -- foveolar hyperplasia -- gastric -- invasion -- metaplasia -- MUC4 -- SPEM; Histochemistry -- Periodicals; Cytochemistry -- Periodicals; Histocytochemistry -- methods; Histological Techniques; 572.05
• DOI: 10.1369/0022155418785621
• Languages: English
• ISSNs: 0022-1554

Abstract

Gastric adenocarcinoma develops in metaplastic mucosa associated with Helicobacter pylori infection in the stomach. We have sought to evaluate the precise lineage changes in the stomachs of insulin-gastrin (INS-GAS) mice infected with H. pylori and/or intestinal flora (Altered Schaedler's Flora; ASF). Stomachs from groups infected with H. pylori contained progressive spasmolytic polypeptide-expressing metaplasia (SPEM) compared with germ-free and mice infected with ASF alone. The overall phenotype of the H. pylori -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 H. pylori 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 H. pylori /ASF-infected mouse expressed both UEAI and Muc4 . Finally, we identified an increase in the number of tuft cells within the mucosa of H. pylori -infected groups. Our findings suggest that H. pylori 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.