So keep your mouth healthy.
The readable article here:
New study helps explain why a cleaner mouth could mean a healthier heart
The abstract/research here:
- Published: May 4, 2015
- DOI: 10.1371/journal.pone.0125126
Abstract
There
is strong epidemiological association between periodontal disease and
cardiovascular disease but underlying mechanisms remain ill-defined.
Because the human periodontal disease pathogen,
Porphyromonas gingivalis
(Pg), interacts with innate immune receptors Toll-like Receptor (TLR) 2
and CD36/scavenger receptor-B2 (SR-B2), we studied how CD36/SR-B2 and
TLR pathways promote Pg-mediated atherosclerosis. Western diet fed low
density lipoprotein receptor knockout (
Ldlr°) mice infected
orally with Pg had a significant increase in lesion burden compared with
uninfected controls. This increase was entirely CD36/SR-B2-dependent,
as there was no significant change in lesion burden between infected and
uninfected
Ldlr° mice. Western diet feeding promoted enhanced
CD36/SR-B2-dependent IL1β generation and foam cell formation as a result
of Pg lipopolysaccharide (PgLPS) exposure. CD36/SR-B2 and TLR2 were
necessary for inflammasome activation and optimal IL1ß generation, but
also resulted in LPS induced lethality (pyroptosis). Modified forms of
LDL inhibited Pg-mediated IL1ß generation in a CD36/SR-B2-dependent
manner and prevented pyroptosis, but promoted foam cell formation. Our
data show that Pg infection in the oral cavity can lead to significant
TLR2-CD36/SR-B2 dependent IL1ß release. In the vessel wall, macrophages
encountering systemic release of IL1ß, PgLPS and modified LDL have
increased lipid uptake, foam cell formation, and release of IL1ß,
but
because pyroptosis is inhibited, this enables macrophage survival and
promotes increased plaque development. These studies may explain
increased lesion burden as a result of periodontal disease, and suggest
strategies for development of therapeutics.
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