Restoring gut bacteria to youthful age linked to improved stroke recovery in mice
http://circres.ahajournals.org/content/120/2/249?etoc=
There
continues to be a rapidly evolving interest in the role of the gut
microbiome in cardiovascular disease. It has long been known that the
gut microbiome has a fundamentally mutualistic, symbiotic relationship
with the human host. However, from earlier observations using mice grown
in germ-free environments to more recent advances in identifying unique
metabolic products of the gut microbiome,1
the data have led to a compelling story linking cardiovascular disease
to the trillions of prokaryotic organisms that live in the human gut.
Article, see p 312
In this issue of Circulation Research, Santisteban et al2
have provided provocative data demonstrating very definitively that, in
2 different animal models of hypertension, there is decreased
expression of several tight junction proteins in the gut and a
concomitant increase in intestinal permeability. Furthermore, their data
show that in the spontaneously hypertensive rat model, the increase in
permeability is a result of increased sympathetic nerve activity before
the development of hypertension. They therefore conclude that there is a
direct, causal link between the sympathetic nerve activity derived from
the central nervous system and increased gut permeability (Figure).
They further hypothesize that the changes in gut permeability result in
hypertension and cause a shift in the types of bacteria that are
present in the gut. Finally, they have shown that the changes in
sympathetic activity resulting in increased gut permeability are also
associated with an increase in inflammatory cells within the intestinal
wall thus potentially bringing the contributions of the immune system to
hypertension into this pathophysiological mechanism.
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