ArticleWorld journal of gastroenterology2005
Helicobacter pylori upregulates prion protein expression in gastric mucosa: a possible link to prion disease.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Effect of Two Different Drug-ResistantFrontiers in veterinary science · 2022Article
- Prion protein PrP nucleic acid binding and mobilization implicates retroelements as the replicative component of transmissible spongiform encephalopathy.Archives of virology · 2020Review
- Binding between Prion Protein and Aβ Oligomers Contributes to the Pathogenesis of Alzheimer's Disease.Virologica Sinica · 2019Review
- Amyloid-β Activates Microglia and Regulates Protein Expression in a Manner Similar to Prions.Journal of molecular neuroscience : MN · 2015Article
- Article
- PrP106-126 and Aβ 1-42 peptides induce BV-2 microglia chemotaxis and proliferation.Journal of molecular neuroscience : MN · 2014Article
- Article
- Bacterial colitis increases susceptibility to oral prion disease.The Journal of infectious diseases · 2009Article
- Prion stability and infectivity in the environment.Neurochemical research · 2009Review
- Regulation of prion protein expression: a potential site for therapeutic intervention in the transmissible spongiform encephalopathies.International journal of biomedical science : IJBS · 2006Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimPathological 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.
methodsWe 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 was analyzed in gastric cell lines.
resultsPrPc 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.
conclusionH 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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