Unraveling the key to the resistance of canids to prion diseases
Fig 7
Brain analyses from RML, 301C and 22L inoculated mice.
A. Two mouse brains from each inoculated group (Tg402, Tg403 and C57BL/6) were selected to determine the presence of protease-K (PK) resistant PrP. Samples were treated with 85 μg/ml of PK and protease resistant protein was analyzed by Western blot using SAF-83 (1:400) monoclonal antibody. Only C57BL/6 inoculated brain samples showed characteristic PK-resistant PrP migration patterns. All transgenic mouse brains were devoid of all PK-resistant PrP. C(Mo): undigested mouse brain homogenate. B. Histopathological characterization of different mouse prion strains (RML, 301C and 22L) inoculated intracerebrally in Tg402, Tg403 and C57BL/6 wild-type mice. Two mouse-adapted scrapie derived strains (RML and 22L) and a mouse-adapted BSE derived strain (301C) showed typical spongiform change only in the brains of wild-type mice in hematoxylin and eosin (H&E) stained sections. No TSE-related lesions were observed in Tg402 nor in Tg403 inoculated mice with any of the strains. Similarly, upon immunohistochemical labeling with 6H4 antibody against prion protein [PrPres IHC (6H4)] (1:1,000), only the wild-type mice had immunolabeled deposits of prion protein. All images were taken at the same magnification in the region of the diencephalon. WT: Wild-type. Bar 50 μm.