Vestnik Moskovskogo universiteta Seria 16 Biologia,
Journal Year:
2024,
Volume and Issue:
79(№4, 2024), P. 315 - 321
Published: Jan. 1, 2024
Systemic
chronic
inflammation
(SCI)
can
develop
due
to
diabetes
mellitus,
coronary
artery
disease,
atherosclerosis,
autoimmune
diseases,
kidney,
liver,
and
lung
pathologies,
cancer,
etc.
During
the
COVID-19
pandemic,
there
was
clear
evidence
showing
that
damages
endothelial
cells
of
vascular
wall,
leading
impaired
microcirculation.
Currently,
mechanisms
causing
pathological
changes
in
brain
amid
SCI
are
still
unclear.
In
this
work,
we
investigated
how
systemic
affects
vasodilatory
function
cerebral
arteries.
modeled
using
well-established
cecal
ligation
puncture
model,
which
involves
tying
off
cecum
below
ileocecal
valve
puncturing
it
with
a
needle.
For
characterizing
model
animals,
recorded
body
weight,
blood
pressure,
analyzed
levels
leukocytes,
ESR,
hematocrit,
erythrocyte
aggregation
arterial
blood,
number
desquamated
venous
blood.
The
density
network
pial
membrane
reactivity
studied
vivo
microvascular
imaging.
vessels
per
unit
area
diameter
under
influence
vasoactive
substances
–
aminoguanidine
(an
inducible
NO-synthase
inhibitor)
acetylcholine
were
measured.
From
7
days
3
months
after
onset
SCI,
leukocyte
rat
increased
by
2.1–1.7
times
compared
control
group.
1.8
control.
Erythrocyte
rose
an
average
1.3
times.
decreased
1.7
constrictions
arteries
induced
1.5
3.7
expanded
response
4.9
Thus,
over
period
three
leads
decrease
deterioration
vasomotor
American Journal of Transplantation,
Journal Year:
2024,
Volume and Issue:
24(5), P. 724 - 732
Published: Feb. 10, 2024
Acute-on-chronic
liver
failure
is
a
well-established
description
of
high
mortality
syndrome
chronic
disease
(usually
cirrhosis)
with
organ
failure.
While
the
exact
definition
under
refinement
accepted
understanding
this
entity
in
patients
who
have
various
organs
and
where
systemic
inflammation
major
component
pathobiology.
There
are
limited
therapies
for
such
poor
prognosis
while
improvements
critical
care
management
very
few
patients,
transplantation,
mean
50%
can
survive
to
hospital
discharge,
rapid
application
new
required.
Here
we
explain
current
immunological
abnormalities
seen
ACLF
across
innate
adaptive
immune
systems,
role
hepatic
cell
death
gut
axis
recommendations
future
research
treatment
paradigms.
Liver International,
Journal Year:
2024,
Volume and Issue:
unknown
Published: April 9, 2024
Abstract
Accurate
prediction
of
survival
in
patients
with
cirrhosis
is
crucial,
as
who
are
unlikely
to
survive
the
short‐term
need
be
oriented
liver
transplantation
and
novel
therapeutic
approaches.
Patients
acute
decompensation
without
or
organ
dysfunction/failure,
so‐called
acute‐on‐chronic
failure
(ACLF),
have
a
particularly
high
mortality.
Recognizing
specificity
this
clinical
situation,
dedicated
classifications
scores
been
developed
over
last
15
years,
including
variables
(e.g.
failures
systemic
inflammation)
not
part
formerly
available
severity
scores,
namely
Child‐Pugh
score
MELD.
For
cirrhosis,
it
led
development
score,
Clif‐C‐AD
independently
validated.
more
severe
patients,
three
different
scoring
systems
proposed,
by
European,
Asian
North
American
societies
Clif‐C‐ACLF,
AARC
NASCELD‐ACLF
respectively.
These
validated,
widely
used
across
world.
The
differences
similarities
between
these
well
their
validation
limitations
discussed
here.
Even
if
step
forward
favouring
homogeneity
studies,
helping
making
decisions
for
individual
predictive
value
mortality
can
still
improved
area
under
ROC
curve
does
exceed
.8.
Novel
biomarkers
reflecting
pathophysiology
might
help
reach
that
goal.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(4), P. 2073 - 2073
Published: Feb. 8, 2024
Acute-on-chronic
liver
failure
(ACLF)
is
a
syndrome
marked
by
sudden
function
decline
and
multiorgan
failure,
predominantly
acute
kidney
injury
(AKY),
in
patients
with
chronic
disease.
Unregulated
inflammation
hallmark
of
ACLF;
however,
the
key
drivers
ACLF
are
not
fully
understood.
This
study
explores
therapeutic
properties
human
mesenchymal
stem
cell
(MSC)
secretome,
particularly
focusing
on
its
enhanced
anti-inflammatory
pro-regenerative
after
vitro
preconditioning
cells.
We
evaluated
efficacy
systemic
administration
MSC
secretome
preventing
AKI
rat
model
where
disease
was
induced
using
porcine
serum,
followed
D-galN/LPS
to
induce
failure.
After
induction,
animals
were
treated
saline
(ACLF
group)
or
MSC-derived
(ACLF-secretome
group).
The
revealed
that
MSC-secretome
strongly
reduced
histological
damage
group,
which
correlated
higher
hepatocyte
proliferation,
increased
hepatic
molecule
levels,
neutrophil
macrophage
infiltration.
Additionally,
renal
examination
treatment
mitigated
tubular
injuries,
apoptosis,
downregulated
markers.
These
improvements
linked
survival
rates
ACLF-secretome
endorsing
secretomes
as
promising
therapy
for
ACLF.
Background:
Liver
failure
profoundly
affects
the
immune
system,
leading
to
dysregulation
of
innate
and
adaptive
responses.
Body:
This
review
explores
intricate
relationship
between
liver
function
homeostasis.
The
role
as
a
central
hub
in
response
initiation
is
elucidated,
emphasizing
its
involvement
hepatic
inflammation
induction
subsequent
systemic
inflammation.
Cytokines,
chemokines,
growth
factors,
lipid
mediators
orchestrate
these
processes,
serving
both
prognostic
biomarkers
potential
therapeutic
targets
failure-associated
dysregulation.
Furthermore,
delves
into
mechanisms
underlying
immunosuppression
failure,
encompassing
alterations
cell
functions
such
neutrophils,
macrophages,
natural
killer
cells
(NK
cells),
well
perturbations
responses
mediated
by
B
T
cells.
Conclusion:
Understanding
immunological
consequences
crucial
for
developing
targeted
interventions
improving
patient
outcomes
disease
management.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(17), P. 9522 - 9522
Published: Sept. 1, 2024
Liver
failure
profoundly
affects
the
immune
system,
leading
to
dysregulation
of
innate
and
adaptive
response.
This
review
explores
intricate
relationship
between
liver
function
homeostasis.
The
role
as
a
central
hub
in
response
initiation
is
elucidated,
emphasizing
its
involvement
hepatic
inflammation
induction
subsequent
systemic
inflammation.
Cytokines,
chemokines,
growth
factors,
lipid
mediators
orchestrate
these
processes,
serving
both
prognostic
biomarkers
potential
therapeutic
targets
failure-associated
dysregulation,
which
might
result
from
acute-on-chronic
(ACLF)
cirrhosis.
Furthermore,
delves
into
mechanisms
underlying
immunosuppression
failure,
encompassing
alterations
cell
functions
such
neutrophils,
macrophages,
natural
killer
cells
(NK
cells),
well
perturbations
responses
mediated
by
B
T
cells.
Conclusion:
Understanding
immunological
consequences
crucial
for
developing
targeted
interventions
improving
patient
outcomes
disease
management.
Gastroenterología y Hepatología,
Journal Year:
2024,
Volume and Issue:
47(10), P. 502207 - 502207
Published: May 8, 2024
This
is
the
summary
report
of
5th
Translational
Hepatology
Meeting,
endorsed
by
Spanish
Association
for
Study
Liver
(AEEH)
and
held
in
Seville,
Spain,
October
2023.
The
meeting
aimed
to
provide
an
update
on
latest
advances
field
basic
translational
hepatology,
covering
different
molecular,
cellular,
pathophysiological
aspects
most
relevant
clinical
challenges
liver
pathologies.
includes
identification
novel
biomarkers
diagnostic
tools,
understanding
relevance
immune
response
inflammation
diseases,
characterization
current
medical
approaches
reverse
incorporation
molecular
insights
through
omics
techniques,
or
impact
toxic
metabolic
insults,
as
well
other
organ
crosstalk,
pathophysiology.
Este
es
el
informe
resumen
de
la
5ª
Reunión
Hepatología
Traslacional,
organizada
por
Asociación
Española
para
Estudio
del
Hígado
y
celebrada
en
Sevilla,
España,
octubre
La
reunión
tuvo
como
objetivo
proporcionar
una
actualización
sobre
los
últimos
avances
campo
hepatología
básica
traslacional,
cubriendo
diferentes
aspectos
moleculares,
celulares
fisiopatológicos
las
necesidades
clínicas
más
relevantes
patologías
hepáticas.
Esto
incluye
identificación
nuevos
biomarcadores
herramientas
diagnóstico,
comprensión
relevancia
respuesta
inmune
inflamación
enfermedades
hepáticas,
caracterización
nuevas
aproximaciones
revertir
incorporación
conocimientos
moleculares
a
través
enfoques
ómicos,
o
impacto
agentes
tóxicos
alteraciones
metabólicas,
así
interacción
con
otros
órganos,
fisiopatología
hígado.
Acute-on-Chronic
Liver
Failure
(ACLF)
is
an
acute
and
severe
disease
involving
single
or
multiple
organ
failure.
Due
to
the
unclear
pathogenesis,
there
still
a
lack
of
effective
drug
treatment.
Intestinal
microbiota
closely
related
Bile
Acid
(BA)
metabolism.
In
progression
chronic
liver
ACLF,
BA
metabolism
disorder
often
accompanied
by
intestinal
imbalance,
which
affect
one
another
mutually.
This
article
reviewed
role
in
aims
explore
potential
new
targets
for
treatment
ACLF.
With
the
rising
prevalence
of
chronic
liver
disease
worldwide,
incidence
and
acute-on-chronic
failure
(ACLF)
are
increasing
attribute
to
higher
morbidity,
mortality,
healthcare
costs.
Many
such
patients
die
without
being
considered
for
lifesaving
treatment
option
transplantation.
The
underutilization
transplantation
as
a
therapeutic
in
setting
ACLF,
is
due
multiple
reasons;
with
heterogeneity
ACLF
lack
universal
definition
key
players.
Liver
listing
allocation
based
on
MELD
score.
As
now,
we
do
not
know
where
score
stands
regard
defining
prognostication
patients.
This
insight
very
important
efficient
identification
potential
candidates
ACLF.
review
paper
investigates
role
In
light
recent
evidence,
perfect
model
either.
safety
transplantation,
either
deceased
donor
or
living
donor,
among
has
been
debated.
short-term
mortality
rate
created
need
standard
transplant
selection
criterion
these
Based
published
literature,
find
that
three
commonly
used
definitions
may
be
combination
define
sensitivity,
specificity,
futility
propose
an
algorithm
best
identify
urgent
Moreover,
discuss
data
Future
validation
this
multifaceted
approach
could
bridge
gap
between
appropriately
guided
medical
intervention.