Alveolar
macrophages
(AMs)
reside
in
the
lower
airways
and
play
a
crucial
role
lung
health
response
to
sterile
inflammation
infections.
AMs
possess
remarkable
adaptability
different
environmental
challenges
that
can
persist
through
their
memory
capacity
(trained
immunity).
β-glucan
has
been
characterized
as
potent
inducer
of
trained
immunity
by
reprogramming
hematopoietic
stem
cells
(HSCs)
bone
marrow
generating
innate
with
enhanced
responsiveness.
In
present
study,
we
show
systemic
administration
reprograms
alveolar
via
neutrophils
IFNγ
signalling,
Dectin1-independent
manner.
We
furthermore
demonstrate
AM
at
both
transcriptional
metabolic
levels
exacerbate
injury
following
bacterial
(LPS)
or
viral
(polyI:C)
challenges.
These
findings
identify
an
additional
facet
involving
shed
light
on
potential
detrimental
effects
immunity.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(14), С. 7770 - 7770
Опубликована: Июль 16, 2024
Sepsis-induced
multiple
organ
dysfunction
arises
from
the
highly
complex
pathophysiology
encompassing
interplay
of
inflammation,
oxidative
stress,
endothelial
dysfunction,
mitochondrial
damage,
cellular
energy
failure,
and
dysbiosis.
Over
past
decades,
numerous
studies
have
been
dedicated
to
elucidating
underlying
molecular
mechanisms
sepsis
in
order
develop
effective
treatments.
Current
research
underscores
liver
cardiac
along
with
acute
lung
kidney
injuries,
as
predominant
causes
mortality
patients.
This
understanding
sepsis-induced
failure
unveils
potential
therapeutic
targets
for
treatment.
Various
novel
therapeutics,
including
melatonin,
metformin,
palmitoylethanolamide
(PEA),
certain
herbal
extracts,
gut
microbiota
modulators,
demonstrated
efficacy
different
models.
In
recent
years,
focus
has
shifted
anti-inflammatory
antioxidative
agents
exploring
modulation
metabolism
sepsis.
These
approaches
shown
a
significant
impact
preventing
damage
various
animal
models
but
require
further
clinical
investigation.
The
accumulation
this
knowledge
enriches
our
is
anticipated
facilitate
development
strategies
future.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Авг. 5, 2024
Sepsis-induced
acute
lung
injury
(ALI)
is
a
major
cause
of
death
among
patients
with
sepsis
in
intensive
care
units.
By
analyzing
model
sepsis-induced
ALI
using
lipopolysaccharide
(LPS)
and
cecal
ligation
puncture
(CLP),
treatment
methods
strategies
to
protect
against
were
discussed,
which
could
provide
an
experimental
basis
for
the
clinical
ALI.
Recent
studies
have
found
that
imbalance
autophagy,
ferroptosis,
pyroptosis
key
mechanism
triggers
ALI,
regulating
these
mechanisms
can
improve
injuries
caused
by
LPS
or
CLP.
This
article
summarized
reviewed
regulatory
networks
their
important
roles
process
LPS/CLP-induced
sepsis,
discusses
possible
targeted
drugs
above
effects,
describes
dilemma
prospects,
provides
new
perspectives
future
International Journal of General Medicine,
Год журнала:
2025,
Номер
Volume 18, С. 1163 - 1172
Опубликована: Фев. 28, 2025
Understanding
the
dynamic
changes
in
immune
indicators
during
sepsis
and
their
predictive
value
for
Acute
respiratory
distress
syndrome
(ARDS)
is
crucial
improving
patient
outcomes.
This
single-center,
observational
retrospective
study
was
conducted
at
Lishui
Central
Hospital,
Zhejiang
Province.
Patients
diagnosed
with
Sepsis-3
were
categorized
into
non-ARDS
ARDS
groups
based
on
development.
Data
collection
included
demographics,
clinical
data,
parameters.
Immune
parameters
collected
days
1,
3,
7
post-admission.
Multivariate
logistic
regression
analysis
identified
independent
risk
factors
ARDS,
a
nomogram
model
constructed.
The
ability
of
evaluated
using
ROC
curves.
key
nomogram,
including
CD4,
CD8,
Treg,
lymphocyte,
IgG,
IgA
levels
Days
3
7.
On
Day
CD8
(P
<
0.001),
Tregs
=
0.021),
IgG
0.001)
showed
significant
negative
correlations
7,
CD4
lymphocyte
count
similarly
demonstrated
risk.
had
an
AUC
0.998
(95%
CI:
0.997-0.999),
indicating
high
ability.
Early
indicators,
IgA,
Lymphocyte,
predict
development
ICU
patients.
Alveolar
macrophages
(AMs)
reside
in
the
lower
airways
and
play
a
crucial
role
lung
health
response
to
sterile
inflammation
infections.
AMs
possess
remarkable
adaptability
different
environmental
challenges
that
can
persist
through
their
memory
capacity
(trained
immunity).
β-glucan
has
been
characterized
as
potent
inducer
of
central
trained
immunity
by
reprogramming
hematopoietic
stem
cells
(HSCs)
bone
marrow.
In
present
study,
we
show
systemic
administration
induces
peripheral
alveolar
lungs,
Dectin1-independent
manner.
We
furthermore
demonstrate
AM
at
both
transcriptional
metabolic
levels
exacerbate
injury
following
bacterial
(LPS)
or
viral
(polyI:C)
via
neutrophil/IFN-γ
dependent
These
findings
identify
an
additional
facet
involving
shed
light
on
potential
detrimental
effects
immunity.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(19), С. 10734 - 10734
Опубликована: Окт. 5, 2024
Hydrogen
sulfide
(H2S),
as
a
key
gas
signaling
molecule,
plays
an
important
role
in
regulating
various
diseases,
with
appropriate
concentrations
providing
antioxidative,
anti-inflammatory,
and
anti-apoptotic
effects.
The
specific
of
H2S
acute
hypoxic
injury
remains
to
be
clarified.
This
study
focuses
on
the
donor
sodium
hydrosulfide
(NaHS)
explores
its
protective
effects
mechanisms
against
lung
injury.
First,
mouse
hypoxia
models
were
established
evaluate
H2S’s
protection
tolerance.
Next,
rat
model
(ALI)
induced
by
at
6500
m
above
sea
level
for
72
h
was
created
assess
mechanisms.
Evaluation
metrics
included
blood
analysis,
routine
indicators,
water
content,
tissue
pathology.
Additionally,
LC-MS/MS
bioinformatic
analyses
combined
performing
quantitative
proteomics
tissues
from
normoxic
control
group,
group
NaHS
treatment
preliminarily
explore
H2S.
Further,
enzyme-linked
immunosorbent
assays
(ELISA)
used
measure
oxidative
stress
markers
inflammatory
factors
tissues.
Lastly,
Western
blot
analysis
performed
detect
Nrf2,
HO-1,
P-NF-κB,
NF-κB,
HIF-1α,
Bcl-2,
Bax
proteins
Results
showed
that
exhibited
significant
anti-hypoxic
models,
effectively
modulating
indicators
ALI
rats,
reducing
pulmonary
edema,
improving
pathology,
alleviating
stress,
responses,
apoptosis
levels.
The Kaohsiung Journal of Medical Sciences,
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 23, 2024
Abstract
Acute
lung
injury
(ALI)
is
a
common
and
severe
complication
of
sepsis
with
high
mortality
rate.
Ferroptosis,
an
iron‐dependent
form
cell
death,
contributes
to
injury.
Homeobox
A5
(HOXA5)
involved
in
the
regulation
septic
acute
kidney
damage;
however,
its
function
on
ferroptosis
ALI
remains
unclear.
An
vitro
model
was
established
pulmonary
epithelial
line
(MLE‐12)
via
lipopolysaccharide
(LPS)
stimulation.
Cell
viability,
ferrous
iron
(Fe
2+
)
level,
cellular
lipid
reactive
oxygen
species
(ROS)
were
determined
Counting
Kit‐8
assay,
assay
kit,
BODIPY™
665/676
molecular
probe,
respectively.
HOXA5,
suppressor
protein
1
(FSP1),
sirtuin
5
(SIRT5),
glutathione
peroxidase
4
(GPX4)
expressions
measured
using
western
blotting
Real‐Time
Quantitative
Polymerase
Chain
Reaction
(RT‐qPCR.
Chromatin
immunoprecipitation
luciferase
reporter
assays
performed
validate
HOXA5
binding
FSP1/GPX4
promoter,
SIRT5
desuccinylation
confirmed
through
co‐immunoprecipitation.
LPS
stimulation
induced
(reduced
elevated
Fe
ROS
levels,
decreased
GPX4
levels)
downregulated
FSP1
levels.
overexpression
neutralized
LPS‐induced
ferroptosis.
Moreover,
exposure
inhibited
which
counteracted
overexpression.
Furthermore,
suppressed
In
LPS‐challenged
MLE‐12
cells,
SIRT5‐mediated
reduced.
depletion
suppressive
role
by
upregulating
FSP1,
may
offer
prospective
therapeutic
strategy
for
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Сен. 3, 2024
ABSTRACT
Alveolar
macrophages
(AMs)
reside
in
the
lower
airways
and
play
a
crucial
role
lung
health
response
to
sterile
inflammation
infections.
AMs
possess
remarkable
adaptability
different
environmental
challenges
that
can
persist
through
their
memory
capacity
(trained
immunity).
β-glucan
has
been
characterized
as
potent
inducer
of
trained
immunity
by
reprogramming
hematopoietic
stem
cells
(HSCs)
bone
marrow
generating
innate
with
enhanced
responsiveness.
In
present
study,
we
show
systemic
administration
reprograms
alveolar
via
neutrophils
IFNγ
signalling,
Dectin1-independent
manner.
We
furthermore
demonstrate
AM
at
both
transcriptional
metabolic
levels
exacerbate
injury
following
bacterial
(LPS)
or
viral
(polyI:C)
challenges.
These
findings
identify
an
additional
facet
involving
shed
light
on
potential
detrimental
effects
immunity.
