Huntington's
disease
(HD)
is
a
currently
incurable
neurogenerative
disorder
and
typically
characterized
by
progressive
movement
(including
chorea),
cognitive
deficits
(culminating
in
dementia),
psychiatric
abnormalities
(the
most
common
of
which
depression),
peripheral
symptoms
gastrointestinal
dysfunction).
There
are
no
approved
disease‐modifying
therapies
available
for
HD,
with
death
usually
occurring
approximately
10–25
years
after
onset,
but
some
hold
promising
potential.
HD
subjects
often
burdened
chronic
diarrhea,
constipation,
esophageal
gastric
inflammation,
susceptibility
to
diabetes.
Our
understanding
the
microbiota–gut–brain
axis
its
infancy
growing
evidence
from
preclinical
clinical
studies
suggests
role
gut
microbial
population
imbalance
(gut
dysbiosis)
pathophysiology.
The
brain
can
communicate
through
enteric
nervous
system,
immune
vagus
nerve,
microbiota‐derived‐metabolites
including
short‐chain
fatty
acids,
bile
branched‐chain
amino
acids.
This
review
summarizes
supporting
demonstrating
alterations
bacterial
fungal
composition
that
may
be
associated
HD.
We
focus
on
mechanisms
dysbiosis
compromise
health,
thus
triggering
neuroinflammatory
responses,
further
highlight
outcomes
attempts
modulate
microbiota
as
therapeutic
strategies
Ultimately,
we
discuss
dearth
data
need
more
longitudinal
translational
this
nascent
field.
suggest
future
directions
improve
our
association
between
microbes
pathogenesis
other
‘brain
body
disorders’.
Cells,
Год журнала:
2023,
Номер
12(5), С. 793 - 793
Опубликована: Март 2, 2023
The
gut
microbiota,
including
bacteria,
archaea,
fungi,
viruses
and
phages,
inhabits
the
gastrointestinal
tract.
This
commensal
microbiota
can
contribute
to
regulation
of
host
immune
response
homeostasis.
Alterations
have
been
found
in
many
immune-related
diseases.
metabolites
generated
by
specific
microorganisms
such
as
short-chain
fatty
acids
(SCFAs),
tryptophan
(Trp)
bile
acid
(BA)
metabolites,
not
only
affect
genetic
epigenetic
but
also
impact
metabolism
cells,
immunosuppressive
inflammatory
cells.
cells
(such
tolerogenic
macrophages
(tMacs),
dendritic
(tDCs),
myeloid-derived
suppressive
(MDSCs),
regulatory
T
(Tregs),
B
(Breg)
innate
lymphocytes
(ILCs))
Macs
(iMacs),
DCs,
CD4
helper
(Th)1,
CD4Th2,
Th17,
natural
killer
(NK)
NK
neutrophils)
express
different
receptors
for
SCFAs,
Trp
BA
from
microorganisms.
Activation
these
promotes
differentiation
function
inhibits
causing
reprogramming
local
systemic
system
maintain
homeostasis
individuals.
We
here
will
summarize
recent
advances
understanding
effects
on
homeostasis,
especially
functions
Molecular Neurodegeneration,
Год журнала:
2022,
Номер
17(1)
Опубликована: Июнь 17, 2022
A
consequence
of
our
progressively
ageing
global
population
is
the
increasing
prevalence
worldwide
age-related
cognitive
decline
and
dementia.
In
absence
effective
therapeutic
interventions,
identifying
risk
factors
associated
with
becomes
increasingly
vital.
Novel
perspectives
suggest
that
a
dynamic
bidirectional
communication
system
between
gut,
its
microbiome,
central
nervous
system,
commonly
referred
to
as
microbiota-gut-brain
axis,
may
be
contributing
factor
for
health
disease.
However,
exact
mechanisms
remain
undefined.
Microbial-derived
metabolites
produced
in
gut
can
cross
intestinal
epithelial
barrier,
enter
systemic
circulation
trigger
physiological
responses
both
directly
indirectly
affecting
functions.
Dysregulation
this
(i.e.,
dysbiosis)
modulate
cytotoxic
metabolite
production,
promote
neuroinflammation
negatively
impact
cognition.
review,
we
explore
critical
connections
microbial-derived
(secondary
bile
acids,
trimethylamine-N-oxide
(TMAO),
tryptophan
derivatives
others)
their
influence
upon
function
neurodegenerative
disorders,
particular
interest
less-explored
role
decline.
Frontiers in Immunology,
Год журнала:
2022,
Номер
13
Опубликована: Фев. 3, 2022
Inflammatory
bowel
disease
(IBD)
is
a
chronic
immune-mediated
inflammatory
disorder
of
the
gastrointestinal
tract
that
arises
due
to
complex
interactions
between
host
genetic
risk
factors,
environmental
and
dysbiotic
gut
microbiota.
Although
metagenomic
approaches
have
attempted
characterise
dysbiosis
occurring
in
IBD,
precise
mechanistic
pathways
interlinking
microbiota
intestinal
mucosa
are
still
yet
be
unravelled.
To
deconvolute
these
interactions,
more
reductionist
approach
involving
microbial
metabolites
has
been
suggested.
Bile
acids
emerged
as
key
class
microbiota-associated
perturbed
IBD
patients.
In
recent
years,
metabolomics
studies
revealed
consistent
defect
bile
acid
metabolism
with
an
increase
primary
reduction
secondary
This
review
explores
evolving
evidence
specific
interact
epithelial
immune
cells
contribute
milieu
seen
IBD.
Furthermore,
we
summarise
linking
intracellular
known
relevant
including
autophagy,
apoptosis,
inflammasome
pathway.
Finally,
discuss
how
novel
experimental
bioinformatics
could
further
advance
our
understanding
role
inform
therapeutic
strategies
Antibiotics
(ABX)
compromise
the
efficacy
of
programmed
cell
death
protein
1
(PD-1)
blockade
in
cancer
patients,
but
mechanisms
underlying
their
immunosuppressive
effects
remain
unknown.
By
inducing
down-regulation
mucosal
addressin
adhesion
molecule
(MAdCAM-1)
ileum,
post-ABX
gut
recolonization
by
Enterocloster
species
drove
emigration
enterotropic
α4β7+CD4+
regulatory
T
17
cells
into
tumor.
These
deleterious
ABX
were
mimicked
oral
gavage
species,
genetic
deficiency,
or
antibody-mediated
neutralization
MAdCAM-1
and
its
receptor,
α4β7
integrin.
contrast,
fecal
microbiota
transplantation
interleukin-17A
prevented
ABX-induced
immunosuppression.
In
independent
lung,
kidney,
bladder
patient
cohorts,
low
serum
levels
soluble
had
a
negative
prognostic
impact.
Thus,
MAdCAM-1-α4β7
axis
constitutes
an
actionable
immune
checkpoint
immunosurveillance.
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(15), С. 8343 - 8343
Опубликована: Июль 28, 2022
The
digestive
tract
is
replete
with
complex
and
diverse
microbial
communities
that
are
important
for
the
regulation
of
multiple
pathophysiological
processes
in
humans
animals,
particularly
those
involved
maintenance
intestinal
homeostasis,
immunity,
inflammation,
tumorigenesis.
diversity
bile
acids
a
result
joint
efforts
host
microflora.
There
bidirectional
relationship
between
community
that,
while
flora
tightly
modulates
metabolism
synthesis
acids,
acid
pool
composition
affect
homeostasis
flora.
Homeostatic
imbalances
systems
may
lead
to
development
variety
diseases,
such
as
inflammatory
bowel
disease
(IBD),
colorectal
cancer
(CRC),
hepatocellular
carcinoma
(HCC),
type
2
diabetes
(T2DM),
polycystic
ovary
syndrome
(PCOS).
interactions
be
(in)directly
pathogenesis
these
diseases.
Signal Transduction and Targeted Therapy,
Год журнала:
2023,
Номер
8(1)
Опубликована: Дек. 6, 2023
Gut-liver-brain
axis
is
a
three-way
highway
of
information
interaction
system
among
the
gastrointestinal
tract,
liver,
and
nervous
systems.
In
past
few
decades,
breakthrough
progress
has
been
made
in
gut
liver
brain
axis,
mainly
through
understanding
its
formation
mechanism
increasing
treatment
strategies.
this
review,
we
discuss
various
complex
networks
including
barrier
permeability,
hormones,
microbial
metabolites,
vagus
nerve,
neurotransmitters,
immunity,
toxic
β-amyloid
(Aβ)
metabolism,
epigenetic
regulation
gut-liver-brain
axis.
Some
therapies
containing
antibiotics,
probiotics,
prebiotics,
synbiotics,
fecal
microbiota
transplantation
(FMT),
polyphenols,
low
FODMAP
diet
nanotechnology
application
regulate
Besides,
some
special
treatments
targeting
gut-liver
include
farnesoid
X
receptor
(FXR)
agonists,
takeda
G
protein-coupled
5
(TGR5)
glucagon-like
peptide-1
(GLP-1)
antagonists
fibroblast
growth
factor
19
(FGF19)
analogs.
Targeting
gut-brain
embraces
cognitive
behavioral
therapy
(CBT),
antidepressants
tryptophan
metabolism-related
therapies.
liver-brain
contains
Aβ
future,
better
interactions
will
promote
development
novel
preventative
strategies
discovery
precise
therapeutic
targets
multiple
diseases.
