Abstract
Inflammatory
bowel
disease
(IBD)
is
a
chronic
disorder
linked
to
an
increased
risk
of
colorectal
cancer
(CRC)
and
characterized
by
significant
dysbiosis
in
the
gut
microbiota.
The
commensal
bacterium
Parabacteroides
goldsteinii
(
P.
)
has
shown
potential
modulating
host
metabolism
inflammatory
responses.
In
this
study,
we
investigated
probiotic
properties
its
mechanism
action
IBD
models,
with
particular
focus
on
bile
acid
diet‐microbiota
interactions.
Fecal
samples
from
patients
ulcerative
colitis
n
=
14),
Crohn's
22),
healthy
controls
13)
were
analyzed
assess
relative
abundance.
dextran
sulfate
sodium
(DSS)‐induced
azoxymethane
(AOM)/DSS‐induced
CRC
mouse
administration
significantly
attenuated
inflammation
tumorigenesis,
particularly
under
fiber‐free
diet
conditions.
Metabolomic
profiling
revealed
enrichment
secondary
acids
‐treated
mice,
suggesting
link
between
anti‐inflammatory
effects.
Further
mechanistic
studies
using
salt
hydrolase
inhibitors
Tgr5
knockout
mice
confirmed
role
regulation
mediating
therapeutic
benefits
.
Additionally,
found
that
dietary
factors
influenced
colonization
metabolic
activity
,
thereby
efficacy.
This
highlights
for
microbiome‐based
therapies
tailored
specific
contexts
treatment
IBD.
Our
findings
demonstrate
can
modulate
alleviate
colitis,
making
it
promising
candidate
applications
management,
modulation
enhancing
potential.
Trends in Microbiology,
Год журнала:
2024,
Номер
32(12), С. 1229 - 1240
Опубликована: Июнь 5, 2024
Recent
studies
of
dynamic
interactions
between
epigenetic
modifications
a
host
organism
and
the
composition
or
activity
its
associated
gut
microbiota
suggest
an
opportunity
for
to
shape
microbiome
through
alterations
that
lead
changes
in
gene
expression
noncoding
RNA
activity.
We
use
insights
from
microbiota-induced
review
potential
epigenetically
regulate
microbiome,
which
bidirectional
'epigenome–microbiome
axis'
emerges.
This
axis
embeds
environmentally
induced
variation,
may
influence
adaptive
evolution
host–microbe
interactions.
furthermore
present
our
perspective
on
how
epigenome–microbiome
can
be
understood
investigated
within
holo-omic
framework
with
applications
applied
health
food
sciences.
Cell Host & Microbe,
Год журнала:
2024,
Номер
32(6), С. 820 - 836
Опубликована: Июнь 1, 2024
Microbial
communities
that
colonize
the
human
gastrointestinal
(GI)
tract
defend
against
pathogens
through
a
mechanism
known
as
colonization
resistance
(CR).
Advances
in
technologies
such
next-generation
sequencing,
gnotobiotic
mouse
models,
and
bacterial
cultivation
have
enhanced
our
understanding
of
underlying
mechanisms
intricate
microbial
interactions
involved
CR.
Rather
than
being
attributed
to
specific
clades,
CR
is
now
understood
arise
from
dynamic
interplay
between
microbes
host
shaped
by
metabolic,
immune,
environmental
factors.
This
evolving
perspective
underscores
significance
contextual
factors,
encompassing
microbiome
composition
conditions,
determining
review
highlights
recent
research
has
shifted
its
focus
toward
elucidating
how
these
factors
interact
either
promote
or
impede
enteric
infections.
It
further
discusses
future
directions
unravel
complex
relationship
host,
microbiota,
determinants
safeguarding
GI
infections
health.
Gut,
Год журнала:
2024,
Номер
73(11), С. 1909 - 1920
Опубликована: Июль 13, 2024
The
gut
microbiome
has
been
recognised
as
a
key
component
in
the
pathogenesis
of
inflammatory
bowel
diseases
(IBD),
and
wide
range
metabolites
produced
by
bacteria
are
an
important
mechanism
which
human
interacts
with
host
immunity
or
metabolism.
High-throughput
metabolomic
profiling
novel
computational
approaches
now
allow
for
comprehensive
assessment
thousands
diverse
biomaterials,
including
faecal
samples.
Several
groups
metabolites,
short-chain
fatty
acids,
tryptophan
bile
have
associated
IBD.
In
this
Seminars in Immunopathology,
Год журнала:
2025,
Номер
47(1)
Опубликована: Март 4, 2025
Abstract
Understanding
the
role
of
gut
microbiota
in
pathogenesis
inflammatory
bowel
diseases
(IBD)
has
been
an
area
intense
research
over
past
decades.
Patients
with
IBD
exhibit
alterations
their
microbial
composition
compared
to
healthy
controls.
However,
studies
focusing
solely
on
taxonomic
analyses
have
struggled
deliver
replicable
findings
across
cohorts
regarding
which
species
drive
distinct
patterns
IBD.
The
focus
therefore
shifted
studying
functionality
microbes,
especially
by
investigating
effector
molecules
involved
immunomodulatory
functions
microbiota,
namely
metabolites.
Metabolic
profiles
are
altered
IBD,
and
several
metabolites
shown
play
a
causative
shaping
immune
animal
models.
Therefore,
understanding
complex
communication
between
metabolites,
host
bears
great
potential
unlock
new
biomarkers
for
diagnosis,
disease
course
therapy
response
as
well
novel
therapeutic
options
treatment
In
this
review,
we
primarily
promising
classes
thought
exert
beneficial
effects
generally
decreased
Though
results
from
human
trials
promising,
they
not
so
far
provided
large-scale
break-through
IBD-therapy
improvement.
We
propose
tailored
personalized
supplementation
based
multi-omics
analysis
accounts
individual
metabolic
patients
rather
than
one-size-fits-all
approaches.
Abstract
Rheumatoid
arthritis
(RA)
is
an
autoimmune
disease.
Early
studies
hold
opinion
that
gut
microbiota
environmentally
acquired
and
associated
with
RA
susceptibility.
However,
accumulating
evidence
demonstrates
genetics
also
shape
the
microbiota.
It
known
some
strains
of
inbred
laboratory
mice
are
highly
susceptible
to
collagen-induced
(CIA),
while
others
resistant
CIA.
Here,
we
show
transplantation
fecal
CIA-resistant
C57BL/6J
CIA-susceptible
DBA/1J
confer
CIA
resistance
in
mice.
healthy
human
individuals
have
enriched
B.
fragilis
than
patients.
Transplantation
prevents
We
identify
mainly
produces
propionate
higher
level
propionate.
Fibroblast-like
synoviocytes
(FLSs)
activated
undergo
tumor-like
transformation.
Propionate
disrupts
HDAC3-FOXK1
interaction
increase
acetylation
FOXK1,
resulting
reduced
FOXK1
stability,
blocked
interferon
signaling
deactivation
RA-FLSs.
treat
attenuates
Moreover,
a
combination
anti-TNF
etanercept
synergistically
relieves
These
results
suggest
or
could
be
alternative
complementary
approach
current
therapies.
