NR AWNI
AU Scherbel,C.; Pichner,R.; Groschup,M.H.; Mueller-Hellwig,S.; Scherer,S.; Maertlbauer,E.; Gareis,M.
TI Influence of bovine gastrointestinal microbiota on scrapie associated prion protein (PrPsc)
QU International Conference - Prion 2006: Strategies, advances and trends towards protection of society - 3.10.-6.10.2006, Torino, Italy, Lingotto Conference Centre - Poster sessions RA-11
PT Konferenz-Poster
AB The influence of complex microflora residing in the gastrointestinal tract of cattle on prion protein plays a crucial role with respect to early pathogenesis and the potential infectivity of faeces resulting in environmental contamination. However, it is unknown whether infectious prion proteins, considered to be very stable, are inactivated by microbial processes in the gastrointestinal tract of animals. Feedstuffs consumed by ruminants are initially exposed to microbial fermentation in the rumen prior to gastric and intestinal digestion. Especially the polygastric digestion of ruminants represents an efficient system to degrade food proteins by microbial fermentation processes in rumen and colon. In this study, rumen and colon contents from healthy cattle, taken immediately after slaughter, were used to assess the ability of these microbial consortia to inactivate PrPsc. Therefore, the consortia were incubated with brain homogenates of scrapie (strain 263K) infected hamsters under physiological anaerobic conditions. Recently, studies were published indicating the ability of complex ruminal and colonic microbiota of cattle to decrease scrapie associated prion protein up to immunochemically undetectable levels in Western blot under physiological conditions. Subsequently, comparatively analysing the concomitance of the loss of anti-prion antibody 3F4 immunoreactivity and the inactivation of PrPsc in vivo hamster bioassays were performed. However, the results demonstrated significant prion infectivity after degradation of infected hamster brain through the gastrointestinal microflora of cattle. Thus, infectivity is still present and may enter the host, irrespectively of the mechanism, by PrPsc at levels below the threshold of immunochemical detection, or by a sub-fraction of infectious prion protein not detectable by immunochemical methods. Finally, the possibility of present infectious molecules or structures other than PrPsc must be seriously considered. Conclusively, these data highlight the deficiency of using Western blot or immunoassay formats in TSE inactivation assessment studies, and raise the possibility that the environment might be contaminated through cattle shedding infected faeces.
AD C. Scherbel, R. Pichner, M. Gareis: Institute for Microbiology and Toxicology, Federal Research Centre for Nutrition and Food, Kulmbach, Germany; M.H. Groschup: Institute for Novel and Emerging Diseases, Friedrich-Loeffler-Institute, Isle of Riems, Germany; S. Mueller-Hellwig, S. Scherer: Unit of Microbiology, Central Research Institute for Nutrition and Food, Technical University Munich, Germany; E. Maertlbauer: Institute for Hygiene and Technology of Milk, Veterinary Faculty, Ludwig-Maximilians University, Munich, Germany. E-mail: Christina.Scherbel@bfel.de
SP englisch
PO Italien