ArticleThe Journal of infectious diseases2009
Bacterial colitis increases susceptibility to oral prion disease.
Article in The Journal of infectious diseases, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Exosomes in Amyloid Propagation-Roles in Neurodegeneration.Molecular neurobiology · 2026Review
- Bovine Spongiform Encephalopathy: An Integrated Review of Prion Mechanisms, Neuroanatomy, and Control.Veterinary sciences · 2026Review
- Alterations in gut microbiota linked to provenance, sex, and chronic wasting disease in white-tailed deer (Odocoileus virginianus).Scientific reports · 2021Article
- Oxazolone-induced gastrointestinal disorders enhance the oral transmission of AA amyloidosis in mice.The Journal of veterinary medical science · 2021Article
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- Oral Ingestion of Synthetically Generated Recombinant Prion Is Sufficient to Cause Prion Disease in Wild-Type Mice.Pathogens (Basel, Switzerland) · 2020Article
- Cellular and Molecular Mechanisms of Prion Disease.Annual review of pathology · 2019Review
- Oral Prion Neuroinvasion Occurs Independently of PrPJournal of virology · 2018Article
- How do PrPPathogens (Basel, Switzerland) · 2017Review
- Prion disease pathogenesis in the absence of the commensal microbiota.The Journal of general virology · 2017Article
- Increased Abundance of M Cells in the Gut Epithelium Dramatically Enhances Oral Prion Disease Susceptibility.PLoS pathogens · 2016Article
- The Gut-Associated Lymphoid Tissues in the Small Intestine, Not the Large Intestine, Play a Major Role in Oral Prion Disease Pathogenesis.Journal of virology · 2015Article
- Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory Case-Control Study.British journal of medicine and medical research · 2014Article
- The immunobiology of prion diseases.Nature reviews. Immunology · 2013Review
- Prion disease and the innate immune system.Viruses · 2012Review
- B cell-specific S1PR1 deficiency blocks prion dissemination between secondary lymphoid organs.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- M cell-depletion blocks oral prion disease pathogenesis.Mucosal immunology · 2012Article
- Endogenous prion protein attenuates experimentally induced colitis.The American journal of pathology · 2011Article
- Protein aggregation diseases: pathogenicity and therapeutic perspectives.Nature reviews. Drug discovery · 2010Review
- Pathogenesis of natural goat scrapie: modulation by host PRNP genotype and effect of co-existent conditions.Veterinary researchArticle
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 4 countries.
Funding
Abstract
Dietary exposure to prion-contaminated materials has caused kuru and variant Creutzfeldt-Jakob disease in humans and transmissible spongiform encephalopathies (TSEs) in cattle, mink, and felines. The epidemiology of dietary prion infections suggests that host genetic modifiers and possibly exogenous cofactors may play a decisive role in determining disease susceptibility. However, few cofactors influencing susceptibility to prion infection have been identified. In the present study, we investigated whether colitis might represent one such cofactor. We report that moderate colitis caused by an attenuated Salmonella strain more than doubles the susceptibility of mice to oral prion infection and modestly accelerates the development of disease after prion challenge. The prion protein was up-regulated in intestines and mesenteric lymph nodes of mice with colitis, providing a possible mechanism for the effect of colitis on the pathogenesis of prion disease. Therefore, moderate intestinal inflammation at the time of prion exposure may constitute one of the elusive risk factors underlying the development of TSE.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.