Abstract | AIM: Pathological prion protein (PrP(sc)) is responsible for the development of transmissible spongiform encephalopathies (TSE). While PrPc enters the organism via the oral route, less data is available to know about its uptake and the role of gastrointestinal inflammation on the expression of prion precursor PrPc, which is constitutively expressed in the gastric mucosa. METHODS: RESULTS: PrPc expression was increased in H pylori- infection compared with non-infected controls and decreased to normal after successful eradication. Gastrin, PGE(2), and IL-1beta dose-dependently upregulated PrPc in gastric cells, while TNF-alpha had no effect. CONCLUSION: H pylori infection leads to the upregulation of gastric PrPc expression. This can be linked to H pylori induced hypergastrinemia and increased mucosal PGE(2) and IL-1beta synthesis. H pylori creates a milieu for enhanced propagation of prions in the gastrointestinal tract.
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Authors | Peter C Konturek, Karolina Bazela, Vitaliy Kukharskyy, Michael Bauer, Eckhart G Hahn, Detlef Schuppan |
Journal | World journal of gastroenterology
(World J Gastroenterol)
Vol. 11
Issue 48
Pg. 7651-6
(Dec 28 2005)
ISSN: 1007-9327 [Print] United States |
PMID | 16437693
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Interleukin-1
- Prions
- RNA, Messenger
- Tumor Necrosis Factor-alpha
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Topics |
- Adult
- Aged
- Cell Line
- Gastric Mucosa
(metabolism)
- Helicobacter Infections
(metabolism)
- Helicobacter pylori
(pathogenicity)
- Humans
- Interleukin-1
(pharmacology)
- Middle Aged
- Prion Diseases
(etiology)
- Prions
(biosynthesis)
- RNA, Messenger
(analysis)
- Tumor Necrosis Factor-alpha
(pharmacology)
- Up-Regulation
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