Interleukin-17A Promotes Parietal Cell Atrophy by Inducing Apoptosis
Cellular and Molecular Gastroenterology and Hepatology, ISSN: 2352-345X, Vol: 5, Issue: 4, Page: 678-690.e1
2018
- 42Citations
- 174Usage
- 39Captures
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Metrics Details
- Citations42
- Citation Indexes42
- 42
- CrossRef30
- Usage174
- Downloads166
- Abstract Views8
- Captures39
- Readers39
- 39
Article Description
Atrophic gastritis caused by chronic inflammation in the gastric mucosa leads to the loss of gastric glandular cells, including acid-secreting parietal cells. Parietal cell atrophy in a setting of chronic inflammation induces spasmolytic polypeptide expressing metaplasia, a critical step in gastric carcinogenesis. However, the mechanisms by which inflammation causes parietal cell atrophy and spasmolytic polypeptide expressing metaplasia are not well defined. We investigated the role of interleukin-17A (IL-17A) in causing parietal cell atrophy. A mouse model of autoimmune atrophic gastritis was used to examine IL-17A production during early and late stages of disease. Organoids derived from corpus glands were used to determine the direct effects of IL-17A on gastric epithelial cells. Immunofluorescent staining was used to examine IL-17A receptors and the direct effect of signaling on parietal cells. Mice were infected with an IL-17A-producing adenovirus to determine the effects of IL-17A on parietal cells in vivo. Finally, IL-17A neutralizing antibodies were administered to mice with active atrophic gastritis to evaluate the effects on parietal cell atrophy and metaplasia. Increased IL-17A correlated with disease severity in mice with chronic atrophic gastritis. IL-17A caused caspase-dependent gastric organoid degeneration, which could not be rescued with a necroptosis inhibitor. Parietal cells expressed IL-17A receptors and IL-17A treatment induced apoptosis in parietal cells. Overexpressing IL-17A in vivo induced caspase-3 activation and terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling staining in parietal cells. Finally, IL-17A neutralizing antibody decreased parietal cell atrophy and metaplasia in mice with chronic atrophic gastritis. These data identify IL-17A as a cytokine that promotes parietal cell apoptosis during atrophic gastritis, a precursor lesion for gastric cancer.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2352345X17301911; http://dx.doi.org/10.1016/j.jcmgh.2017.12.012; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85044612233&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/29930985; https://linkinghub.elsevier.com/retrieve/pii/S2352345X17301911; https://digitalcommons.wustl.edu/open_access_pubs/6846; https://digitalcommons.wustl.edu/cgi/viewcontent.cgi?article=7854&context=open_access_pubs; https://dx.doi.org/10.1016/j.jcmgh.2017.12.012
Elsevier BV
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