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From: TSS ()
Subject: Expression of Prion Protein in the Gut of Mice Infected Orally with the 301V Murine Strain of the BSE Agent
Date: May 18, 2005 at 6:02 pm PST

-------- Original Message --------
Subject: Expression of Prion Protein in the Gut of Mice Infected Orally with the 301V Murine Strain of the BSE Agent
Date: Tue, 17 May 2005 17:09:32 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@aegee.org


##################### Bovine Spongiform Encephalopathy #####################

1: J Comp Pathol. 2005 May;132(4):273-82.


Expression of Prion Protein in the Gut of Mice Infected Orally with
the 301V Murine Strain of the Bovine Spongiform Encephalopathy Agent.

Gonzalez L, Terry L, Jeffrey M.

Veterinary Laboratories Agency (VLA-Lasswade), Pentlands Science
Park, Midlothian EH26 0PZ, UK.

Transmissible spongiform encephalopathies (TSEs) are characterized
by the accumulation of an abnormal, disease-associated prion protein
(PrP(d)). Expression of its normal cellular counterpart (PrP(c)) by
the host is a pre-requisite for the spread of infection to the
central nervous system and the development of disease. Moreover,
cells expressing PrP(c) at specific sites such as the
gastrointestinal tract might be regarded as the initial point of
PrP(c)-PrP(d) conversion after infection by the oral route. In this
study, inbred mice of the I/M strain were infected orally with the
301V murine strain of the bovine spongiform encephalopathy agent.
The expression of PrP(c) and the accumulation of PrP(d) in the
intestine was then investigated immunohistochemically, together with
the variations in immunoreactivity that resulted from different
pretreatments of the tissue. After proteinase K (PK) pretreatment,
abnormal PrP was still detectable only in the gut-associated
lymphoid tissue (GALT) of clinically affected mice and, to a much
more limited degree, in the enteric nervous system (ENS). Cellular
PrP that disappeared after PK treatment was particularly conspicuous
in the ENS and present to a lesser extent in the GALT of all mice
examined after inoculation with 301V or with normal brain
homogenates, as well as in uninoculated controls. These findings
suggested that not all PrP found in infected mice was PrP(d) and
that part of the PrP(d) was sensitive to PK treatment. Reactivity to
PrP antibody 1A8 was consistently found in the absorptive epithelium
of the intestinal villi, with or without PK pretreatment. However,
epithelial immunolabelling was comparable in inoculated and
uninoculated mice and was also consistently seen in PrP "knockout"
mice used as controls. It is therefore concluded that
immunohistochemically detectable accumulation of PrP(d) in the gut
of mice is a relatively late event in the pathogenesis of
experimental infection in this model and that the immunoreactivity
observed in the intestinal epithelium does not correspond to PrP
expression. While enterocytes may still play a role in the uptake of
infection from the intestinal lumen, the results do not suggest that
these cells are a site of initial accumulation of PrP(d).

PMID: 15893985 [PubMed - in process]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15893985

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