How Brain Cells are Killed During Lyme Disease
Mort Zuckerman
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Subject: How Brain Cells are Killed During Lyme Disease
Date: Nov 19, 2009 7:42 PM
ARTICLE BELOW
=========================
WHEREAS, according to IDSociety.org, "Lyme
Disease" is only "an autoimmune arthritis in
a knee caused by cross-reacting antibodies
to OspA - the vaccine - and T cells,"...
...this'n here other kinda disease, which
IDSA calls "We-Don't-Know-What-You-Have Disease,:"
http://www.actionlyme.org/Schoen.htm
(See ^^^Yale's Robert Schoen tell an MD
I never met nor heard of, that "Kathleen
Dickson has I-Don't-Know Disease"), is
revealed to be caused by 2 extra, coordinating
cells wherein the third cell, the brain cell
or nerve dies.
We don't know what causes Yale to have
We-Don't-Know Disease, but we, the ones
with the dead-brain-cells, think we
may know why Yale has We-Don't-Know:
The complicating variable known
as US Patent 6,045,804:
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6045804.PN.&OS=PN/6045804&RS=PN/6045804
"The vaccine don't work, and seems
to cause an identical illness to..."
you guessed it... "We-Don't-Know Disease."
==========================================
http://www.ncbi.nlm.nih.gov/pubmed?term=19911057[uid]&cmd=DetailsSearch&log$=details
Microglia are mediators of Borrelia burgdorferi-induced apoptosis in
SH-SY5Y neuronal cells.
Myers TA, Kaushal D, Philipp MT.
Division of Bacteriology & Parasitology, Tulane National Primate
Research Center, Tulane University Health Sciences Center, Louisiana,
United States of America.
Inflammation has long been implicated as a contributor to pathogenesis
in many CNS illnesses, including Lyme neuroborreliosis. Borrelia
burgdorferi is the spirochete that causes Lyme disease and it is known
to potently induce the production of inflammatory mediators in a
variety of cells. In experiments where B. burgdorferi was co-cultured
in vitro with primary microglia, we observed robust expression and
release of IL-6 and IL-8, CCL2 (MCP-1), CCL3 (MIP-1alpha), CCL4
(MIP-1beta) and CCL5 (RANTES), but we detected no induction of
microglial apoptosis. In contrast, SH-SY5Y (SY) neuroblastoma cells co-
cultured with B. burgdorferi expressed negligible amounts of
inflammatory mediators and also remained resistant to apoptosis. When
SY cells were co-cultured with microglia and B. burgdorferi,
significant neuronal apoptosis consistently occurred. Confocal
microscopy imaging of these cell cultures stained for apoptosis and
with cell type-specific markers confirmed that it was predominantly
the SY cells that were dying. Microarray analysis demonstrated an
intense microglia-mediated inflammatory response to B. burgdorferi
including up-regulation in gene transcripts for TLR-2 and NFkappabeta.
Surprisingly, a pathway that exhibited profound changes in regard to
inflammatory signaling was triggering receptor expressed on myeloid
cells-1 (TREM1). Significant transcript alterations in essential p53
pathway genes also occurred in SY cells cultured in the presence of
microglia and B. burgdorferi, which indicated a shift from cell
survival to preparation for apoptosis when compared to SY cells
cultured in the presence of B. burgdorferi alone. Taken together,
these findings indicate that B. burgdorferi is not directly toxic to
SY cells; rather, these cells become distressed and die in the
inflammatory surroundings generated by microglia through a bystander
effect. If, as we hypothesized, neuronal apoptosis is the key
pathogenic event in Lyme neuroborreliosis, then targeting microglial
responses may be a significant therapeutic approach for the treatment
of this form of Lyme disease.
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci
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