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From: TSS (216-119-143-226.ipset23.wt.net)
Subject: New molecular markers of early and progressive CJD brain infection
Date: January 24, 2005 at 5:07 pm PST

-------- Original Message --------
Subject: New molecular markers of early and progressive CJD brain infection
Date: Mon, 24 Jan 2005 11:07:46 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


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

Fast Track
New molecular markers of early and progressive CJD brain infection
Zhi Yun Lu, Christopher A. Baker, Laura Manuelidis *
Yale Medical School, New Haven, Connecticut 06510
email: Laura Manuelidis (laura.manuelidis@yale.edu
)

*Correspondence to Laura Manuelidis, Yale Medical School, FMB 11, 333
Cedar Street, New Haven, CT 06510.

Funded by:
National Institutes of Health; Grant Number: NS12674
United States Department of Defense; Grant Number: DAMD 17-03-1-0360

Keywords

host recognition " innate immunity " RT-PCR " diagnosis " TSE agents "
prion

Abstract

Transmissible spongiform encephalopathies (TSEs), including human
Creutzfeldt-Jakob disease (CJD), are caused by a related group of
infectious agents that can be transmitted to many mammalian species.
Because the infectious component of TSE agents has not been identified,
we examined myeloid cell linked inflammatory pathways to find if they
were activated early in CJD infection. We here identify a specific set
of transcripts in CJD infected mouse brains that define early and later
stages of progressive disease. Serum amyloid A3 and L-selectin mRNAs
were elevated as early as 20 days after intracerebral inoculation.
Transcripts of myeloid cell recruitment factors such as MIP-1 , MIP-1 ,
and MCP1, as well as IL1 and TNF were upregulated >10 fold between 30
and 40 days, well before prion protein (PrP) abnormalities that begin
only after 80 days. At later stages of symptomatic neurodegenerative
disease (100-110 days), a selected set of transcripts rose by as much as
100 fold. In contrast, normal brain inoculated controls showed no
similar sequential changes. In sum, rapid and simple PCR tests defined
progressive stages of CJD brain infection. These markers may also
facilitate early diagnosis of CJD in accessible peripheral tissues such
as spleen and blood. Because some TSE strains can differentially target
particular cell types such as microglia, several of these molecular
changes may also distinguish specific agent strains. The many host
responses to the CJD agent challenge the assumption that the immune
system does not recognize TSE infections because these agents are
composed only of the host's own PrP. © 2004 Wiley-Liss, Inc.

------------------------------------------------------------------------
Received: 11 May 2004; Accepted: 14 June 2004

Digital Object Identifier (DOI)


10.1002/jcb.20220 About DOI


http://www3.interscience.wiley.com/cgi-bin/abstract/109585596/ABSTRACT

TSS

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





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