Epstein-Barr virus Infection Exacerbates Ulcerative Colitis by Driving Macrophage Pyroptosis via the Upregulation of Glycolysis
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.
Language: Английский
Gut virome and its implications in the pathogenesis and therapeutics of inflammatory bowel disease
Yushan Wu,
No information about this author
Rui Cheng,
No information about this author
Hao Lin
No information about this author
et al.
BMC Medicine,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: March 26, 2025
Language: Английский
Akkermansia muciniphila Protects Against Trinitrobenzene Sulfonic Acid Induced Colitis by Inhibiting IL6/STAT3 Pathway
Mingshan Jiang,
No information about this author
Yongbin Jia,
No information about this author
Chunxiang Ma
No information about this author
et al.
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.
Language: Английский