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Interleukin-17A Promotes Parietal Cell Atrophy by Inducing Apoptosis
Kevin A Bockerstett1, Luciana H Osaki2, Christine P Petersen3
1Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St Louis, Missouri.
Cellular and Molecular Gastroenterology and Hepatology
|June 23, 2018
Summary
Interleukin-17A (IL-17A) drives parietal cell apoptosis in atrophic gastritis, a key step in gastric cancer development. Neutralizing IL-17A reduces this cell loss and metaplasia in mice.
Area of Science:
- Gastroenterology
- Immunology
- Oncology
Background:
- Atrophic gastritis involves chronic inflammation and loss of gastric parietal cells.
- Parietal cell loss leads to metaplasia, a precursor to gastric cancer.
- Mechanisms linking inflammation to parietal cell atrophy are not fully understood.
Purpose of the Study:
- To investigate the role of interleukin-17A (IL-17A) in parietal cell atrophy.
- To elucidate the mechanisms by which IL-17A contributes to gastric carcinogenesis.
Main Methods:
- Used a mouse model of autoimmune atrophic gastritis to study IL-17A production.
- Examined IL-17A effects on gastric organoids and parietal cells in vitro.
- Assessed IL-17A receptor expression and in vivo effects using adenovirus and neutralizing antibodies.
Main Results:
- Increased IL-17A levels correlated with atrophic gastritis severity in mice.
- IL-17A induced caspase-dependent apoptosis in parietal cells and gastric organoids.
- IL-17A neutralizing antibodies reduced parietal cell atrophy and metaplasia.
Conclusions:
- IL-17A promotes parietal cell apoptosis in atrophic gastritis.
- IL-17A is a significant factor in gastric carcinogenesis progression.
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