Two Studies Not Performed by UConn/Yale Having the Utmost Importance re Childrens Health
Mort Zuckerman
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Subject: Two Studies Not Performed by UConn/Yale Having the Utmost
Importance re Childrens Health
Date: May 14, 2010 12:42 PM
1) Susceptibility to sepsis (severe infections)
via TLR2 polymorphisms, and
2) TLR2-Agonist related neurodevelopmental
damage.
Yale and UConn can't discuss childhood
diseases or developmental disabilities
because they still haven't admitted what
OspA does/is, LOL.
This is not to mention the epidemic
of asthma caused by molds, which is
the opposite of the OspA-Mold-induced immune
dyregulation outcomes: Leukemia, Lupus, MS,
Chronic Fatigue, etc.
(It's not surprising that the UConn
pretzeldink bolted as soon as he could.)
KMDickson
http://www.actionlyme.org
=============================
http://www.ncbi.nlm.nih.gov/pubmed/20456021
J Neurochem. 2010 Apr 29. [Epub ahead of print]
TLR2 Activation Inhibits Embryonic Neural Progenitor Cell
Proliferation.
Okun E, Griffioen KJ, Gen-Son T, Lee JH, Roberts NJ, Mughal MR,
Hutchison E, Cheng A, Arumugam TV, Lathia JD, van Praag H, Mattson MP.
Laboratory of Neurosciences, National Institute on Aging Intramural
Research Program, Baltimore, Maryland 21224, U.S.A.
Abstract
Abstract Toll-like receptors (TLRs) play essential roles in innate
immunity, and increasing evidence indicates that these receptors are
expressed in neurons, astrocytes and microglia in the brain, where
they mediate responses to infection, stress and injury. To address the
possibility that TLR2 heterodimer activation could affect progenitor
cells in the developing brain, we analyzed the expression of TLR2
throughout the mouse cortical development, and assessed the role of
TLR2 heterodimer activation in neural progenitor cell (NPC)
proliferation. TLR2 mRNA and protein was expressed in the cortex in
embryonic and early postnatal stages of development, and in cultured
cortical NPC. While NPC from TLR2-deficient and wild type embryos had
the same proliferative capacity, TLR2 activation by the synthetic
bacterial lipopeptides Pam(3)CSK(4) and FSL1, or low molecular weight
hyaluronan, an endogenous ligand for TLR2, inhibited neurosphere
formation in vitro. Intracerebral in utero administration of TLR2
ligands resulted in ventricular dysgenesis characterized by increased
ventricle size, reduced proliferative area around the ventricles,
increased cell density, an increase in PH3 (+) cells and a decrease in
BrdU(+) cells in the sub-ventricular zone. Our findings indicate that
loss of TLR2 does not result in defects in cerebral development.
However, TLR2 is expressed and functional in the developing
telencephalon from early embryonic stages and infectious agent-related
activation of TLR2 inhibits NPC proliferation. TLR2-mediated
inhibition of NPC proliferation may therefore be a mechanism by which
infection, ischemia and inflammation adversely affect brain
development.
PMID: 20456021 [PubMed - as supplied by publisher]
=======================
http://www.ncbi.nlm.nih.gov/pubmed/20463618
Pediatr Res. 2010 May 11. [Epub ahead of print]
Role of Polymorphic Variants as Genetic Modulators of Infection in
Neonatal Sepsis.
Abu-Maziad A, Schaa K, Bell EF, Dagle JM, Cooper M, Marazita ML,
Murray JC.
Department of Pediatrics [A.A.-M., K.S., E.F.B., J.M.D., J.C.M.]
University of Iowa, Children's Hospital, Iowa City, Iowa, 52242;
Department of Pediatrics [A.A-M.], Suez Canal University, Ismailia
41522, Egypt; Center for Craniofacial and Dental Genetics [M.C.,
M.L.M.], University of Pittsburgh, Pittsburgh, Pennsylvania, 15219.
Abstract
This study is a retrospective, case-control study involving 535
preterm infants examining the roles of sequence polymorphisms in genes
that mediate host immune responses to bacterial infection in newborn
infants. A total of 49 single nucleotide polymorphisms (SNPs) in 19
candidate genes including inflammatory cytokines (IL6, IL10, IL1B,
TNF), cytokine receptors (IL1RN), toll-like receptors (TLR2, TLR4,
TLR5) and cell surface receptors (CD14) were genotyped. Subjects were
stratified into 3 groups (sepsis, suspected sepsis, control). The data
were analyzed using a family-based transmission disequilibrium test.
We found that birth weight, gestational age, duration of rupture of
membranes, and presence of clinical chorioamnionitis were strongly
associated with sepsis. Polymorphisms in TLR2 (rs3804099), TLR5
(rs5744105), IL10 (rs1800896), and PLA2G2A (rs1891320) genes were
associated with sepsis. Allelic variants in PLA2G2A and TLR2 were
associated with Gram-positive infections, while IL10 was associated
with Gram-negative infections (p< 0.05). We conclude allelic
variations in PLA2G2A, TLR2, TLR5, and IL10 may moderate the
predisposition to sepsis in preterm infants. ABBREVIATIONS::
PMID: 20463618 [PubMed - as supplied by publisher]
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