OspA (LYMErix) "contributes to vascular leakage" - New on MedLine :)))
Kathleen
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Subject: OspA (LYMErix) "contributes to vascular leakage" - New on
MedLine :)))
Date: Dec 28, 2010 6:33 AM
There ya go. More proof LYMErix
could not have been a vaccine,
meaning Steere et al, must be
lying about SOMETHING...
Oh, and you can ask Brian
Fallon at Columbia about Lyme-brain
and vascular leakage. And about his
4.7 million dollar study that
re-proved that "Lyme Disease" (I
should say Relapsing Fever, and
especially not Pam3Cys Relapsing
Fever) is incurable:
http://www.actionlyme.org/Fallon.htm
http://www.actionlyme.org/FALLON_DANGEROUS_TERRORIST.htm
----------------------------------------
http://www.ncbi.nlm.nih.gov/pubmed/21169547
Bacterial Lipoprotein TLR2 Agonists Broadly Modulate Endothelial
Function and Coagulation Pathways In Vitro and In Vivo.
TLR2 activation induces cellular and organ inflammation and affects
lung function. Because deranged endothelial function and coagulation
pathways contribute to sepsis-induced organ failure, we studied the
effects of bacterial lipoprotein TLR2 agonists, including
peptidoglycan-associated lipoprotein, Pam3Cys, and murein lipoprotein,
on endothelial function and coagulation pathways in vitro and in vivo.
TLR2 agonist treatment induced diverse human endothelial cells to
produce IL-6 and IL-8 and to express E-selectin on their surface,
including HUVEC, human lung microvascular endothelial cells, and human
coronary artery endothelial cells. Treatment of HUVEC with TLR2
agonists caused increased monolayer permeability and had multiple
coagulation effects, including increased production of plasminogen
activator inhibitor-1 (PAI-1) and tissue factor, as well as decreased
production of tissue plasminogen activator and tissue factor pathway
inhibitor. TLR2 agonist treatment also increased HUVEC expression of
TLR2 itself. Peptidoglycan-associated lipoprotein induced IL-6
production by endothelial cells from wild-type mice but not from TLR2
knockout mice, indicating TLR2 specificity. Mice were challenged with
TLR2 agonists, and lungs and plasmas were assessed for markers of
leukocyte trafficking and coagulopathy. Wild-type mice, but not TLR2
mice, that were challenged i.v. with TLR2 agonists had increased lung
levels of myeloperoxidase and mRNAs for E-selectin, P-selectin, and
MCP-1, and they had increased plasma PAI-1 and E-selectin levels.
Intratracheally administered TLR2 agonist caused increased lung fibrin
levels. These studies show that TLR2 activation by bacterial
lipoproteins broadly affects endothelial function and coagulation
pathways, ***suggesting that TLR2 activation contributes in multiple
ways to endothelial activation, coagulopathy, and vascular leakage in
sepsis.***
More on the mechanisms of illness
caused by Pam3Cys or LYMErix:
http://www.actionlyme.org/101016.htm
We find something new every day
because this is reality, despite
lawyers and psychiatrists having
a brain abnormality OKA Cowardice,
with a capital Q (ueer).
KMDickson
http://www.actionlyme.org
http://www.relapsinfever.org