Cell Biology and Toxicology,
Journal Year:
2024,
Volume and Issue:
40(1)
Published: Nov. 11, 2024
As
a
chronic
inflammatory
bowel
disease,
the
pathogenesis
of
ulcerative
colitis
(UC)
has
not
been
fully
elucidated.
N6-methyladenosine
(m6A)
modification,
observed
in
various
RNAs,
is
implicated
diseases.
Methyltransferase-like
14
(METTL14)
major
subunit
methyltransferase
complex
catalyzing
m6A
modifications.
Here,
we
designated
to
examine
regulatory
effects
and
mechanisms
METTL14
on
long
non-coding
RNA
(lncRNA)
during
UC
progression.
knockdown
decreased
cell
viability,
promoted
apoptosis,
increased
cleaved
PARP
Caspase-3
levels,
while
reducing
Bcl-2
levels.
also
led
significant
increase
NF-κB
pathway
activation
cytokine
production
Caco-2
cells
treated
with
TNF-α.
Moreover,
suppression
aggravated
colonic
damage
inflammation
our
dextran
sulfate
sodium
(DSS)-induced
murine
model.
silencing
suppressed
DHRS4-AS1
expression
by
modification
transcripts.
Furthermore,
mitigated
injury
targeting
miR-206/adenosine
A3
receptor
(A3AR)
axis.
overexpression
counteracted
enhancing
impact
TNF-α-induced
cells.
In
conclusion,
findings
suggest
that
protects
against
via
regulating
DHRS4-AS1/miR-206/A3AR
axis,
thus
representing
potential
therapeutic
target
for
UC.
Precision Clinical Medicine,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 21, 2025
Epstein-Barr
virus
(EBV)
infection
is
associated
with
clinical
symptoms,
treatment
response,
need
for
surgical
intervention,
and
an
enhanced
likelihood
of
lymphoma
among
patients
ulcerative
colitis
(UC).
However,
existing
studies
have
primarily
concentrated
on
the
epidemiological
associations
between
EBV
UC,
leaving
mechanisms
by
which
exacerbates
poorly
understood.
Clinical
specimens
UC
a
mouse
model
dextran
sulfate
sodium-induced
concurrent
murine
γ-herpesvirus
68
(MHV-68)
were
utilized
to
investigate
relationship
macrophage
pyroptosis.
In
vivo,
adoptive
transfer
MHV-68-induced
macrophages
depletion
performed
elucidate
underlying
mechanisms.
vitro,
myeloid
leukemia
mononuclear
cells
human
(THP-1)
derived
from
bone
marrow
(BMDMs)
stimulated
MHV-68,
respectively,
assess
pyroptosis
glycolysis.
EBV-induced
activation
was
positively
correlated
disease
activity
in
patients.
Furthermore,
MHV-68
activated
upregulating
gasdermin
D,
NLRP3,
interleukin-1β,
interleukin-18
colonic
tissues
peritoneal
mice
colitis.
also
mediated
THP-1
BMDMs,
respectively.
Additionally,
BMDMs
aggravated
colitis,
whereas
attenuated
intestinal
injury.
Mechanistically,
promoted
glycolysis,
while
glycolysis
inhibitor,
2-deoxy-D-glucose,
blocked
this
process
vitro.
driving
through
upregulation
indicating
potential
therapeutic
approach
mitigate
inflammation.
Journal of Evidence-Based Medicine,
Journal Year:
2024,
Volume and Issue:
17(2), P. 409 - 433
Published: June 1, 2024
Abstract
Inflammatory
bowel
disease
(IBD)
is
a
chronic
and
relapsing
immune‐mediated
of
the
gastrointestinal
tract
with
gradually
increasing
global
incidence
prevalence.
A
prolonged
course
IBD
leads
to
decline
in
patient
quality
life
creation
substantial
economic
burden
on
society.
Owing
lack
specific
diagnostic
markers,
diagnosis
still
needs
gold
standard
based
combination
clinical
manifestations,
imaging,
laboratory,
endoscopic
results.
Accordingly,
current
goals
treatment
are
alleviate
symptoms
reduce
recurrence
rates.
Therefore,
it
imperative
develop
set
procedures
diagnose
treat
IBD.
In
this
review,
we
summarize
prominent
emerging
studies,
outline
classical
contemporary
approaches
diagnosing
managing
IBD,
integrate
multiple
guidelines.
Furthermore,
propose
possibility
establishing
an
early
comprehensive
workflow
personalized
management
strategy
future.
We
aim
enhance
standardization
for
Journal of Translational Medicine,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 13, 2025
The
conversion
of
primary
bile
acids
to
secondary
by
the
gut
microbiota
has
been
implicated
in
colonic
inflammation.
This
study
investigated
role
related
acid
metabolism
inflammation
both
patients
with
inflammatory
bowel
disease
(IBD)
and
a
murine
model
dextran
sulfate
sodium
(DSS)-induced
colitis.
Bile
fecal
samples
from
IBD
DSS-induced
colitis
mice,
without
antibiotic
treatment,
were
analyzed
using
ultraperformance
liquid
chromatography-mass
spectrometry
(UPLC-MS).
composition
DSS-colitis
mice
was
characterized
via
Illumina
MiSeq
sequencing
bacterial
16S
rRNA
gene
V3-V4
region.
Metagenomic
profiling
further
identified
metabolism-related
signatures
stool
mice.
Histological
analysis,
quantitative
PCR
(qPCR)
Western
Blotting
conducted
on
assess
inflammation,
mucosal
barrier
integrity,
associated
signaling
pathways.
multivariate
analysis
Soft
Independent
Modelling
Class
Analogy
(SIMCA,
Umetrics,
Sweden).
relation
between
relative
abundance
specific
phyla/genera
concentration
through
Spearman's
correlation
analyses.
Finally,
lithocholic
(LCA),
key
acid,
administered
gavage
evaluate
its
effect
integrity.
In
IBD,
altered.
Moreover,
changes
modulate
intestine.
As
continues
shift,
profile
undergoes
additional
alterations.
aforementioned
alterations
also
observed
revealed
dysbiosis
modifications
acids,
notably
LCA
Through
as
that
significantly
affects
integrity
barrier.
Subsequent
experiments
confirmed
supplementation
effectively
mitigated
inhibitory
effects
progression
primarily
activation
sphingosine-1-phosphate
receptor
2
(S1PR2)/NF-κB
p65
pathway.
Analysis
microbiome
metagenomic
data
microbiota,
an
increased
unclassified
genus
within
family
Prevotellaceae
Furthermore,
positive
biosynthesis
pathways,
well
level.
These
findings
suggest
positively
correlated
bacteria,
Prevotellaceae,
are
closely
intestinal
Targeting
may
involve
inhibiting
members
potential
therapeutic
strategies.
Frontiers in Oncology,
Journal Year:
2025,
Volume and Issue:
15
Published: March 17, 2025
Inflammation,
a
hallmark
of
cancer,
has
been
associated
with
tumor
progression,
transition
into
malignant
phenotype
and
efficacy
anticancer
treatments
in
cancer.
It
affects
all
stages
from
the
initiation
carcinogenesis
to
metastasis.
Chronic
inflammation
induces
immunosup-pression,
providing
an
environment
conducive
carcinogenesis,
whereas
acute
antitumor
immune
response,
leading
suppression.
Solid
tumors
have
inflammatory
microenvironment
(TME)
containing
cancer
cells,
stromal
soluble
molecules,
which
plays
key
role
progression
therapy
response.
Both
cells
TME
are
highly
plastic
constantly
change
their
phenotypic
functional
properties.
Cancer-associated
inflammation,
majority
consists
innate
important
cell
plasticity,
development
drug
resistance.
Today,
combined
used
advanced
technologies,
such
as
single-cell
RNA
sequencing
spatial
molecular
imaging
analysis,
pathways
linking
chronic
largely
elucidated.
In
this
review
article,
we
highlighted
cellular
mechanisms
involved
cancer-associated
its
effects
on
treatment
We
also
comprehensively
setting
GI
cancers.
DMW - Deutsche Medizinische Wochenschrift,
Journal Year:
2025,
Volume and Issue:
150(08), P. 427 - 432
Published: March 31, 2025
Chronic
inflammatory
bowel
diseases
(IBD),
such
as
Crohn's
disease
(MC)
and
ulcerative
colitis
(CU),
are
serious
immune-mediated
that
affect
the
gastrointestinal
tract
represent
a
considerable
burden
for
patients.
In
recent
decades,
treatment
of
IBD
has
shifted
from
symptomatic
control
to
more
precise,
long-term
goals.
Advances
in
research
have
led
therapy
goals
having
been
redefined
expanded
order
achieve
complete
inflammation
prevent
complications
long
term.An
important
component
modern
therapeutic
approaches
is
definition
specific
markers
serve
indicators
achievement
these
These
enable
objective
monitoring
success
thus
offer
clear
approach
controlling
therapy.
The
present
article
focuses
on
new
discusses
role
target
clinical
practice.A
central
goal
endoscopic
healing,
i.e.
macroscopic
healing
intestinal
mucosa.
practice
this
includes
particular
an
ulcer-free
contrast
remission
alone,
provides
assessment
state
correlates
strongly
with
improved
prognosis.The
histologic
goes
beyond
aims
no
longer
detect
signs
at
microscopic
level.
This
particularly
relevant
results
show
patients
who
histological
even
lower
recurrence
rate
better
than
those
only
or
remission.Even
though
curative
currently
exists,
cure
remains
ultimate
research.
current
practice,
still
unattainable
but
progress
genetic
immunological
offers
hope.
term,
aim
innovative
gene
editing
immunotherapy
disease.
could
mean
not
free
symptoms,
also
freed
term.
Inflammatory Bowel Diseases,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 10, 2025
Abstract
Background
Inflammatory
bowel
disease
is
a
long-standing
inflammatory
disorder
that
influences
the
intestinal
tract.
The
intent
of
this
research
to
explore
whether
relative
abundance
Akkermansia
muciniphila
related
IL6/STAT3
pathway
and
fundamental
molecular
mechanisms
A.
on
trinitrobenzene
sulfonic
acid
(TNBS)-induced
enteritis
mouse
model,
including
expression
cytokines
proteins
in
signaling
pathway.
Methods
association
between
was
investigated
by
using
mucosal
biopsies
fecal
samples.
TNBS-induced
colitis
models
were
performed
elucidate
underlying
mechanisms.
alteration
microbiota
organized
16s
rRNA
sequencing.
Results
In
Crohn’s
patients,
level
STAT3
IL-6
presented
negative
relationship
with
muciniphila.
IL-6,
p-STAT3,
downregulated
A.m+TNBS
group,
indicating
may
inhibit
vivo.
To
investigate
potential
defensive
role
supplementation
vivo
enteritis,
16S
sequencing
analyze
changes
composition.
results
revealed
marked
increase
microbial
diversity
within
muciniphila-treated
suggesting
beneficial
modulation
gut
microbiome
associated
supplementation.
Conclusions
Our
findings
declared
alleviates
gastrointestinal
inflammation
through
IL-6/STAT3
This
protective
effect
mediated
downregulation
STAT3,
highlighting
mechanism
which
modulates
responses.
work
disclosed
demonstrates
influence
against
vivo,
proposing
it
qualified
as
unique
therapeutic
focusing
modulating
or
p-STAT3
treatment
colitis.
Cellular and Molecular Gastroenterology and Hepatology,
Journal Year:
2024,
Volume and Issue:
18(2), P. 101354 - 101354
Published: Jan. 1, 2024
DSS-induced
mouse
colitis
is
caused
by
the
inhibition
of
SIRT1,
leading
to
β-TrCP1
degradation
and
Snail1
stabilization,
resulting
in
disruption
cell
adhesion
tight
junction,
accompanied
integrity
loss
epithelial
barrier
increased
inflammation,
which
can
be
alleviated
NMN.