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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
We studied PrPc expression in the gastric mucosa of 10 Helicobacter pylori-positive patients before and after successful H pylori eradication compared to non-infected controls using RT-PCR and Western blotting. The effect of central mediators of gastric inflammation, i.e., gastrin, prostaglandin E(2) (PGE(2)), tumor necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL-1beta) on PrPc expression
SUBMITTER: Konturek PC
PROVIDER: S-EPMC4727223 | biostudies-literature | 2005 Dec
REPOSITORIES: biostudies-literature