Cerebral targeting indicates vagal spread of infection in hamsters fed with scrapie.

Beekes, Michael; McBride, Patricia; Baldauf, Elizabeth

doi:10.1099/0022-1317-79-3-601

Cited by 205 publications

(157 citation statements)

References 18 publications

(30 reference statements)

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“…Oral challenge of PrP Sc in rodents strongly suggested that infection spread from the gastrointestinal tract via the splanchnic and vagus nerves to the spinal cord and brain [2,3,15,22,23]. Recently, the same result was demonstrated in the cattle after an oral challenge of PrP Sc [12].…”

Section: Discussionsupporting

confidence: 59%

Localization of Sympathetic, Parasympathetic and Sensory Neurons Innervating the Distal Ileum of the Cattle

Ohmori

Atoji

Saito

et al. 2008

The Journal of Veterinary Medical Science

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ABSTRACT. After oral challenge of the pathological prion protein, the causative agent of bovine spongiform encephalopathy, the pathogen was first detected in the distal ileum and then deposited in the brain. The present study aims determining the possible neuronal transporting pathways from the ileum to the brain in the cattle using a tracer protein. After horseradish peroxidase was injected into the wall of the distal ileum in the calf, almost all labeled neurons were detected in the celiac and cranial mesenteric ganglion complex. Only a few labeled neurons existed in the caudal mesenteric ganglion and the paravertebral ganglia. They were sympathetic postganglionic neurons. In the dorsal root ganglia T5 to L4, some sensory neurons were found to be labeled. Only a small number of parasympathetic preganglionic neurons were labeled in the dorsal motor nucleus of the vagus nerve. No labeled sensory neurons were found in the nodose ganglion. These results suggest that the pathological prion protein is mainly transported to the spinal cord and brain via the sympathetic nervous system and partially via the sensory neurons in the dorsal root ganglia. The vagus nerve does not seem to contribute to the transport of the pathogen from the ileum directly. KEY WORDS: autonomic nervous system, cattle, extrinsic innervation, ileum, retrograde labeling.

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Section: Discussionsupporting

confidence: 59%

Localization of Sympathetic, Parasympathetic and Sensory Neurons Innervating the Distal Ileum of the Cattle

Ohmori

Atoji

Saito

et al. 2008

The Journal of Veterinary Medical Science

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“…Following up on experimental pathogenesis studies in mice (16)(17)(18)(19) and sheep (20), the animal model used in this study has provided key observations on the spread of infection through the body (4,(21)(22)(23)(24) that have been confirmed in naturally occurring ovine scrapie (25), field cases of BSE (26), orally transmitted BSE in primates (27), and orally transmitted or naturally occurring CWD (28,29). Additionally, more recent reports on the involvement of the sympathetic nervous system in vCJD (30) and the deposition of PrP Sc in muscles of patients with sporadic CJD (14) have shown the relevance of our hamster model for peripheral PrP Sc routing in TSE-affected humans.…”

Section: Introductionmentioning

confidence: 99%

Preclinical deposition of pathological prion protein PrPSc in muscles of hamsters orally exposed to scrapie

Thomzig¹,

Schulz‐Schaeffer²,

Kratzel³

et al. 2004

J. Clin. Invest.

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Recently, pathological prion protein PrP Sc , the putative key constituent of infectious agents causing transmissible spongiform encephalopathies (TSEs), was found in muscles of rodents experimentally infected with scrapie and in patients with Creutzfeldt-Jakob disease (CJD). For the assessment of risk scenarios originating from these findings (e.g., alimentary transmission of pathogens associated with bovine spongiform encephalopathy [BSE]

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“…Consistent with step-by-step infection of closely apposed cells, prions can multiply and spread along particular neuroanatomical pathways to reach the brain ( [9] and references therein). Extracellular forms of PrP Sc can also be detected in infected tissues [62], the diffusion of which could transmit infection to more distant cells [17].…”

Section: De Novo Infection and Cell-to-cell Dissemination Of Prionsmentioning

confidence: 78%

Cell models of prion infection

Vilette

2007

Vet. Res.

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-Due to recent renewal of interest and concerns in prion diseases, a number of cell systems permissive to prion multiplication have been generated in the last years. These include established cell lines, neuronal stem cells and primary neuronal cultures. While most of these models are permissive to experimental, mouse-adapted strains of prions, the propagation of natural field isolates from sheep scrapie and chronic wasting disease has been recently achieved. These models have improved our knowledge on the molecular and cellular events controlling the conversion of the PrP C protein into abnormal isoforms and on the cell-to-cell spreading of prions. Infected cultured cells will also facilitate investigations on the molecular basis of strain identity and on the mechanisms that lead to neurodegeneration. The ongoing development of new cell models with improved characteristics will certainly be useful for a number of unanswered critical issues in the prion field.

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Cerebral targeting indicates vagal spread of infection in hamsters fed with scrapie.

Cited by 205 publications

References 18 publications

Localization of Sympathetic, Parasympathetic and Sensory Neurons Innervating the Distal Ileum of the Cattle

Localization of Sympathetic, Parasympathetic and Sensory Neurons Innervating the Distal Ileum of the Cattle

Preclinical deposition of pathological prion protein PrPSc in muscles of hamsters orally exposed to scrapie

Cell models of prion infection

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