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Acquired transmissibility of sheep-passaged L-type bovine spongiform encephalopathy prion to wild-type mice.

Okada H, Masujin K, Miyazawa K, Yokoyama T - Vet. Res. (2015)

Bottom Line: Disease-associated prion protein (PrP(Sc)) was detected in the brain and/or lymphoid tissues during the lifespan of mice that were asymptomatic subclinical carriers, indicating that wild-type mice were susceptible to sheep-passaged L-BSE.The morphological characteristics of the PrP(Sc) of sheep-passaged L-BSE included florid plaques that were distributed mainly in the cerebral cortex and hippocampus of subsequent passaged mice.The PrP(Sc) glycoform profiles of wild-type mice infected with sheep-passaged L-BSE were similar to those of the original isolate.

View Article: PubMed Central - PubMed

Affiliation: National Institute of Animal Health, National Agriculture and Food Research Organization (NARO), Tsukuba, Ibaraki, Japan. okadahi@affrc.go.jp.

ABSTRACT
L-type bovine spongiform encephalopathy (L-BSE) is an atypical form of BSE that is transmissible to cattle and several lines of prion protein (PrP) transgenic mice, but not to wild-type mice. In this study, we examined the transmissibility of sheep-passaged L-BSE prions to wild-type mice. Disease-associated prion protein (PrP(Sc)) was detected in the brain and/or lymphoid tissues during the lifespan of mice that were asymptomatic subclinical carriers, indicating that wild-type mice were susceptible to sheep-passaged L-BSE. The morphological characteristics of the PrP(Sc) of sheep-passaged L-BSE included florid plaques that were distributed mainly in the cerebral cortex and hippocampus of subsequent passaged mice. The PrP(Sc) glycoform profiles of wild-type mice infected with sheep-passaged L-BSE were similar to those of the original isolate. The data indicate that sheep-passaged L-BSE has an altered host range and acquired transmissibility to wild-type mice.

No MeSH data available.


Related in: MedlinePlus

Neuroanatomical distribution and morphological patterns of PrPSc accumulation in the brain of ICR mice infected with sheep-passaged L-BSE, at second passage.A The 5 coronal brain sections are as follows: 1. frontal cortex, 2. septal level, 3. hippocampus and thalamic level, 4. midbrain, and 5. medulla with cerebellum. PrP-plaque deposits are abundant throughout the cerebral gray matter (1 to 4) and hippocampus (3 and 4). Granular and aggregated PrPSc accumulated in the septal nuclei (2), hypothalamus (3), and temporal cortex (4). Scale bar = 1 mm. B Histopathology and PrPSc immunohistochemical analysis with mAb SAF84 revealed plentiful florid plaques accompanied by granular and aggregated PrPSc deposits in the hippocampus. Insets show high-magnification images of a florid plaque. Scale bar = 100 μm, scale bar in inset = 25 μm.
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Fig2: Neuroanatomical distribution and morphological patterns of PrPSc accumulation in the brain of ICR mice infected with sheep-passaged L-BSE, at second passage.A The 5 coronal brain sections are as follows: 1. frontal cortex, 2. septal level, 3. hippocampus and thalamic level, 4. midbrain, and 5. medulla with cerebellum. PrP-plaque deposits are abundant throughout the cerebral gray matter (1 to 4) and hippocampus (3 and 4). Granular and aggregated PrPSc accumulated in the septal nuclei (2), hypothalamus (3), and temporal cortex (4). Scale bar = 1 mm. B Histopathology and PrPSc immunohistochemical analysis with mAb SAF84 revealed plentiful florid plaques accompanied by granular and aggregated PrPSc deposits in the hippocampus. Insets show high-magnification images of a florid plaque. Scale bar = 100 μm, scale bar in inset = 25 μm.

Mentions: The inoculum prepared from PrPSc-positive spleens of mice was used for subsequent second passages in ICR mice (Table 1). The long survival period of 691 ± 61 days (n = 6) was statistically unchanged on second passage, without any clinical signs and a 100% transmission rate. Histopathological examination showed prominent florid and non-florid plaques with large confluent vacuoles in the cerebral cortex and hippocampus of all inoculated mice (Figure 2). Florid plaques with a pale central core were generally stained pale basophilic or amphophilic with HE and positively with Congo red under polarized light. A few non-florid plaques were also detected in the thalamus, midbrain tegmentum, and vestibular nucleus. In addition, coarse granular PrPSc and PrPSc aggregates accumulated in the septal nuclei, diagonal band of Broca, hippocampus, hypothalamus, and several limited regions of the cerebral cortex, the olfactory bulb, and the olfactory tract of the frontal cortex (Figure 2B). However, some variation in the intensity of immunolabeling was observed throughout the brain. In addition to the brains of these mice, positive PrPSc immunolabeling was detected in the retina, but not in the spinal cords, trigeminal and dorsal root ganglia, and muscle bundles of skeletal muscle fibers. The pathological results revealed striking differences between first- and second-passaged mice; however the findings from the immunolabeling reactions conducted using the mAbs SAF84, 2G11, and 12F10 for the second-passaged mice were similar to those for the first-passaged mice.Figure 2


Acquired transmissibility of sheep-passaged L-type bovine spongiform encephalopathy prion to wild-type mice.

Okada H, Masujin K, Miyazawa K, Yokoyama T - Vet. Res. (2015)

Neuroanatomical distribution and morphological patterns of PrPSc accumulation in the brain of ICR mice infected with sheep-passaged L-BSE, at second passage.A The 5 coronal brain sections are as follows: 1. frontal cortex, 2. septal level, 3. hippocampus and thalamic level, 4. midbrain, and 5. medulla with cerebellum. PrP-plaque deposits are abundant throughout the cerebral gray matter (1 to 4) and hippocampus (3 and 4). Granular and aggregated PrPSc accumulated in the septal nuclei (2), hypothalamus (3), and temporal cortex (4). Scale bar = 1 mm. B Histopathology and PrPSc immunohistochemical analysis with mAb SAF84 revealed plentiful florid plaques accompanied by granular and aggregated PrPSc deposits in the hippocampus. Insets show high-magnification images of a florid plaque. Scale bar = 100 μm, scale bar in inset = 25 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4499898&req=5

Fig2: Neuroanatomical distribution and morphological patterns of PrPSc accumulation in the brain of ICR mice infected with sheep-passaged L-BSE, at second passage.A The 5 coronal brain sections are as follows: 1. frontal cortex, 2. septal level, 3. hippocampus and thalamic level, 4. midbrain, and 5. medulla with cerebellum. PrP-plaque deposits are abundant throughout the cerebral gray matter (1 to 4) and hippocampus (3 and 4). Granular and aggregated PrPSc accumulated in the septal nuclei (2), hypothalamus (3), and temporal cortex (4). Scale bar = 1 mm. B Histopathology and PrPSc immunohistochemical analysis with mAb SAF84 revealed plentiful florid plaques accompanied by granular and aggregated PrPSc deposits in the hippocampus. Insets show high-magnification images of a florid plaque. Scale bar = 100 μm, scale bar in inset = 25 μm.
Mentions: The inoculum prepared from PrPSc-positive spleens of mice was used for subsequent second passages in ICR mice (Table 1). The long survival period of 691 ± 61 days (n = 6) was statistically unchanged on second passage, without any clinical signs and a 100% transmission rate. Histopathological examination showed prominent florid and non-florid plaques with large confluent vacuoles in the cerebral cortex and hippocampus of all inoculated mice (Figure 2). Florid plaques with a pale central core were generally stained pale basophilic or amphophilic with HE and positively with Congo red under polarized light. A few non-florid plaques were also detected in the thalamus, midbrain tegmentum, and vestibular nucleus. In addition, coarse granular PrPSc and PrPSc aggregates accumulated in the septal nuclei, diagonal band of Broca, hippocampus, hypothalamus, and several limited regions of the cerebral cortex, the olfactory bulb, and the olfactory tract of the frontal cortex (Figure 2B). However, some variation in the intensity of immunolabeling was observed throughout the brain. In addition to the brains of these mice, positive PrPSc immunolabeling was detected in the retina, but not in the spinal cords, trigeminal and dorsal root ganglia, and muscle bundles of skeletal muscle fibers. The pathological results revealed striking differences between first- and second-passaged mice; however the findings from the immunolabeling reactions conducted using the mAbs SAF84, 2G11, and 12F10 for the second-passaged mice were similar to those for the first-passaged mice.Figure 2

Bottom Line: Disease-associated prion protein (PrP(Sc)) was detected in the brain and/or lymphoid tissues during the lifespan of mice that were asymptomatic subclinical carriers, indicating that wild-type mice were susceptible to sheep-passaged L-BSE.The morphological characteristics of the PrP(Sc) of sheep-passaged L-BSE included florid plaques that were distributed mainly in the cerebral cortex and hippocampus of subsequent passaged mice.The PrP(Sc) glycoform profiles of wild-type mice infected with sheep-passaged L-BSE were similar to those of the original isolate.

View Article: PubMed Central - PubMed

Affiliation: National Institute of Animal Health, National Agriculture and Food Research Organization (NARO), Tsukuba, Ibaraki, Japan. okadahi@affrc.go.jp.

ABSTRACT
L-type bovine spongiform encephalopathy (L-BSE) is an atypical form of BSE that is transmissible to cattle and several lines of prion protein (PrP) transgenic mice, but not to wild-type mice. In this study, we examined the transmissibility of sheep-passaged L-BSE prions to wild-type mice. Disease-associated prion protein (PrP(Sc)) was detected in the brain and/or lymphoid tissues during the lifespan of mice that were asymptomatic subclinical carriers, indicating that wild-type mice were susceptible to sheep-passaged L-BSE. The morphological characteristics of the PrP(Sc) of sheep-passaged L-BSE included florid plaques that were distributed mainly in the cerebral cortex and hippocampus of subsequent passaged mice. The PrP(Sc) glycoform profiles of wild-type mice infected with sheep-passaged L-BSE were similar to those of the original isolate. The data indicate that sheep-passaged L-BSE has an altered host range and acquired transmissibility to wild-type mice.

No MeSH data available.


Related in: MedlinePlus