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From: TSS (216-119-144-17.ipset24.wt.net)
Subject: Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions (kidney, pancreas and liver)
Date: January 20, 2005 at 2:14 pm PST

-------- Original Message --------
Subject: Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions
Date: Thu, 20 Jan 2005 16:11:01 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


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

Submitted on October 18, 2004
Accepted on December 6, 2004


Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions

Mathias Heikenwalder 1, Nicolas Zeller 1, Harald Seeger 1, Marco Prinz
2, Peter-Christian Klöhn 3, Petra Schwarz 1, Nancy H. Ruddle 4, Charles
Weissmann 3, Adriano Aguzzi 2*

1 Institute of Neuropathology, University Hospital of Zürich, CH-8091
Zürich, Switzerland.
2 Institute of Neuropathology, University Hospital of Zürich, CH-8091
Zürich, Switzerland; Present address: Institute of Neuropathology,
Georg-August-Universität, D-37073 Göttingen, Germany.
3 Medical Research Council Prion Unit, Department of Neurodegenerative
Diseases, Institute of Neurology, Queen Square, London WC1N 3BG, UK.
4 Department of Epidemiology and Public Health and Section of
Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.

* To whom correspondence should be addressed.
Adriano Aguzzi , E-mail: adriano@pathol.unizh.ch


Prions typically accumulate in nervous and lymphoid tissues. Because
proinflammatory cytokines and immune cells are required for lymphoid
prion replication, we tested whether inflammatory conditions affect
prion pathogenesis. We administered prions to mice with five
inflammatory diseases of kidney, pancreas or liver. In all cases,
chronic lymphocytic inflammation enabled prion accumulation in otherwise
prion-free organs. Inflammatory foci consistently correlated with
lymphotoxin upregulation and ectopic induction of PrPC-expressing
FDC-M1+ cells, whereas inflamed organs of mice lacking
lymphotoxin-{alpha} or its receptor did not accumulate PrPSc nor
infectivity upon prion inoculation. By expanding the tissue distribution
of prions, chronic inflammatory conditions may act as modifiers of
natural and iatrogenic prion transmission.


Science 10.1126/science.1106460
Copyright © 2005 by The American Association for the Advancement of
Science. All rights reserved.


http://www.sciencemag.org/cgi/content/abstract/1106460v1


Illness May Help Mad Cow Agent Spread, Study Finds
Thu Jan 20, 2005 02:09 PM ET


WASHINGTON (Reuters) - The agent that transmits mad cow and related
diseases may spread further in the body of an animal suffering from
certain illnesses, scientists said on Thursday.

Their finding raises the question of whether measures aimed at curbing
the spread of mad cow disease, or bovine spongiform encephalopathy, are
adequate, the researchers said.

Their tests on mice showed that prions, the protein-like fragments that
transmit BSE and related diseases, can show up in organs they are not
supposed to if the mouse has an inflammatory condition.

Scientists have believed that BSE-causing prions are limited to the
brain, spleen, spinal cord and lymph tissue, although some tests have
suggested blood and muscle tissue may also harbor the prions.

The latest study, published in the journal Science, suggests prions may
also sometimes be found in the kidney, pancreas and liver.

"We administered prions to mice with five inflammatory diseases of
kidney, pancreas or liver," wrote the researchers, led by top prion
expert Dr. Adriano Aguzzi of the University Hospital of Zurich in
Switzerland.

Aguzzi and colleagues in Britain and the United States inoculated
specially bred mice with prions and checked to see if the prions spread
in their bodies when the mice had an inflammatory condition. This is
because other studies had suggested that prions might be attracted to
immune system inflammatory cells.

"In all cases, chronic lymphocytic inflammation enabled prion
accumulation in otherwise prion-free organs," the researchers wrote.

BSE peaked in British cattle herds in the mid-1990s and a few cases have
been reported in other countries. Canada reported its third case this
month.

People who eat BSE-infected beef products can develop a related human
brain disease called variant Creutzfeldt-Jakob disease or vCJD. There is
no treatment or cure. It has killed 148 Britons, and five Britons are
alive with the disease, according to the British Department of Health's
monthly report on the disease.

The World Health Organization says it has reports of six cases in
France, one in Ireland, one in Italy, one in Canada and one in the
United States.

Experts believed BSE first appeared when cattle were fed improperly
rendered remains of sheep infected with scrapie, a related disease. In
1997, the United States and Canada imposed animal feed bans, and have
mandated the removal of materials believed to carry infectious prions.

These include the skull, brain, nerves attached to the brain, eyes,
tonsils, spinal cord and attached nerves, plus a portion of the small
intestine.

The study suggests that even symptom-free animals may also have prions
in their livers, kidneys and pancreases.

© Reuters 2005. All Rights Reserved.

http://www.reuters.com/newsArticle.jhtml?type=healthNews&storyID=7385700

TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########





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