Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 14, 2025
Sepsis
is
a
life-threatening
condition
caused
by
dysregulated
host
response
to
infection,
remaining
major
global
health
challenge
despite
clinical
advances.
Therapeutic
challenges
arise
from
antibiotic
misuse,
incomplete
understanding
of
its
complex
pathophysiology,
and
the
unresolved
interplay
immune
dysregulation
microbiota
disruption.
Investigating
microbial
homeostasis
in
shift
cytokine
storm
immunosuppression
may
elucidate
between
metabolites,
dysfunction,
organ
injury,
providing
foundation
for
targeted
therapies
drug
development.
Traditional
Chinese
Medicine
(TCM)
has
demonstrated
significant
advantages
mitigating
sepsis-associated
storms
modulating
gut
homeostasis,
offering
promising
strategy
developing
highly
effective
less
toxic
monomeric
compounds.
Elucidating
interactions
within
immune-inflammation-microbiota
network
sepsis
paves
way
biomarker-driven
personalized
therapeutic
approaches.
American Journal of Respiratory Cell and Molecular Biology,
Journal Year:
2024,
Volume and Issue:
71(4), P. 464 - 480
Published: July 3, 2024
Bronchopulmonary
dysplasia
(BPD)
and
neurodevelopmental
impairment
are
among
the
most
common
morbidities
affecting
preterm
infants.
Although
BPD
is
a
predictor
of
poor
outcomes,
it
currently
uncertain
how
contributes
to
brain
injury
in
Extracellular
vesicles
(EVs)
involved
interorgan
communication
diverse
pathological
processes.
ASC
(apoptosis-associated
speck-like
protein
containing
caspase
recruitment
domain)
pivotal
inflammasome
assembly
activation
inflammatory
response.
We
assessed
expression
profiles
alveolar
macrophage
(AM)
markers
CD11b,
CD11c,
CD206
as
well
EVs
isolated
from
plasma
infants
at
risk
for
1
week
age.
found
that
on
higher
fraction
inspired
oxygen
therapy
(HO
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
15
Published: Jan. 7, 2025
Sepsis-induced
acute
lung
injury
(ALI)
remains
a
leading
cause
of
mortality
in
critically
ill
patients.
Macrophages,
key
modulators
immune
responses,
play
dual
role
both
promoting
and
resolving
inflammation.
Exosomes,
small
extracellular
vesicles
released
by
various
cells,
carry
bioactive
molecules
that
influence
macrophage
polarization
responses.
Emerging
researchers
have
identified
exosomes
as
crucial
mediators
modulate
activity
during
sepsis-induced
ALI.
This
review
explores
the
modulating
functions,
focusing
on
cellular
interactions
within
microenvironment
their
potential
therapeutic
targets.
It
highlights
regulation
macrophages
derived
from
pathogenic
germs,
neutrophils,
alveolar
epithelial
mesenchymal
stromal
cells.
By
understanding
these
mechanisms,
it
aims
to
uncover
innovative
strategies
for
European journal of medical research,
Journal Year:
2025,
Volume and Issue:
30(1)
Published: Jan. 10, 2025
Sepsis
is
characterized
by
an
excessive
immune
response.
Modulation
of
the
response,
particularly
macrophage
polarization,
may
provide
therapeutic
benefit.
The
effects
Caerulomycin
A
(caeA),
a
known
STAT1
phosphorylation
inhibitor,
on
polarization
and
inflammatory
markers
were
explored
using
lipopolysaccharide
(LPS)-induced
sepsis
mouse
model.
model
was
established
in
C57BL/6
mice
induced
intraperitoneal
injection
LPS,
survival
rate
observed
after
treatment
with
different
doses
caeA
to
determine
optimal
dose.
For
in-vitro
assays
RAW264.7
cell
line,
concentration
that
non-toxic
screened
MTT
assay,
followed
analyses
qRT-PCR,
ELISA,
Western
blot
flow
cytometry
for
M1/M2
type
(CD86,
NOS2,
CD206,
ARG1)
factors
(IL-1β,
IL-6,
TNF-α,
IL-4,
IL-10)
expression.
In
addition,
levels
STAT6
JAK–STAT
signaling
pathway
detected.
results
in-vivo
experiments
showed
(20
mg/kg)
significantly
increased
LPS-induced
septic
decreased
expression
M1-type
(CD86
NOS2)
pro-inflammatory
cytokines
TNF-α)
while
increasing
M2-type
(CD206
anti-inflammatory
(IL-4
experiments,
20
μM
effectively
inhibited
macrophages
without
affecting
activity
cells,
yet
enhanced
level
STAT6,
as
detected
blot.
CaeA
modulates
attenuates
response
mice,
possibly
pathway.
These
findings
support
further
exploration
potential
agent
sepsis.
Biomolecules,
Journal Year:
2025,
Volume and Issue:
15(2), P. 174 - 174
Published: Jan. 24, 2025
Inflammation,
a
fundamental
response
to
infection
and
injury,
involves
interactions
among
immune
cells
signaling
molecules.
Dysregulated
inflammation
contributes
diseases
such
as
autoimmune
disorders
cancer.
Interleukin-1
beta
(IL-1β),
produced
by
macrophages
in
lipoteichoic
acid
(LTA)
from
Gram-positive
bacteria,
is
key
inflammatory
mediator.
Glabridin
(GBD),
bioactive
compound
licorice
root,
exhibits
anti-inflammatory
properties.
This
study
investigates
GBD’s
effects
on
LTA-induced
proinflammatory
RAW
264.7
murine
alveolar
macrophages,
MH-S,
focusing
IL-1β
expression
pathways.
Cell
viability
assays
confirmed
that
20
μM
GBD
was
non-cytotoxic.
Confocal
microscopy
quantitative
PCR
showed
significantly
reduced
fluorescence
intensity,
mRNA,
protein
levels.
also
inhibited
inducible
nitric
oxide
synthase
(iNOS)
(NO)
production.
Further
analysis
revealed
suppressed
NF-κB
p65
nuclear
translocation
selectively
modulated
MAPK
pathway
activation
reducing
JNK
p38
phosphorylation
without
affecting
ERK.
Studies
using
specific
inhibitors
demonstrated
production
reduction
mechanistically
linked
inhibition.
These
findings
highlight
potential
therapeutic
agent
for
through
its
ability
modulate
critical
mediators
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Feb. 20, 2025
Sepsis
can
trigger
systemic
inflammation
and
lead
to
detrimental
effects
on
several
organs,
with
particular
emphasis
the
lungs.
In
sepsis-associated
lung
injury,
macrophages
assume
a
pivotal
role,
as
their
overactivation
could
facilitate
secretion
of
inflammatory
factors
imbalance
polarization.
Hepatocyte
nuclear
factor
4
alpha
(HNF4A)
has
been
reported
its
potential
involvement
in
regulation
response
macrophage
This
study
discusses
role
mechanism
HNF4A
sepsis-induced
damage.
exhibits
decrease
expression
by
analyzing
differentially
expressed
genes
lungs
septic
mice
from
Gene
Expression
Omnibus
dataset
GSE15379.
Then,
we
established
mouse
sepsis
model
through
cecal
ligation
puncture
method
observed
that
was
reduced
both
tissues
alveolar
macrophages.
To
evaluate
function
HNF4A,
overexpressed
mediated
adenovirus
vectors,
which
were
injected
into
mice.
We
found
overexpression
resulted
higher
survival
rate
an
amelioration
pulmonary
Meanwhile,
mitigated
infiltration
cells
impeded
M1
polarization
but
facilitated
M2
or
lavage
fluid.
vitro,
treated
bone
marrow-derived
interleukin-4.
Consistent
results
obtained
promoted
Mechanistically,
transcriptionally
regulate
receptor
coactivator
2
(NCOA2)
binding
promoter
region.
NCOA2
interacted
glucocorticoid
(GR).
Stabilin
1
(STAB1)
selected
possible
target
transcriptome
sequencing
analysis.
Functional
experiments
confirmed
STAB1
downstream
HNF4A/NCOA2/GR
axis.
Overall,
this
research
investigated
impact
injury
sepsis.
It
is
suggested
one
regulatory
mechanisms
involved
association
may
be
NCOR2/GR/STAB1