International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(10), P. 9039 - 9039
Published: May 20, 2023
Neutrophil
energy
metabolism
during
phagocytosis
has
been
previously
reported,
and
adenosine
triphosphate
(ATP)
plays
a
crucial
role
in
endocytosis.
Neutrophils
are
prepared
by
intraperitoneal
injection
of
thioglycolate
for
4
h.
We
reported
system
established
measuring
particulate
matter
endocytosis
neutrophils
using
flow
cytometry.
In
this
study,
we
utilized
to
investigate
the
relationship
between
consumption
neutrophils.
A
dynamin
inhibitor
suppressed
ATP
triggered
neutrophil
presence
exogenous
ATP,
behave
differently
depending
on
concentration.
The
inhibition
synthase
nicotinamide
adenine
dinucleotide
phosphate
oxidase
but
not
phosphatidylinositol-3
kinase
suppresses
nuclear
factor
kappa
B
was
activated
inhibited
I
(IKK)
inhibitors.
Notably,
IKK
inhibitors
restored
endocytosis-triggered
consumption.
Furthermore,
data
from
NLR
family
pyrin
domain
containing
three
knockout
mice
suggest
that
inflammasome
activation
is
involved
or
concomitant
To
summarize,
these
molecular
events
occur
via
endocytosis,
which
closely
related
ATP-centered
metabolism.
Journal of Innate Immunity,
Journal Year:
2025,
Volume and Issue:
17(1), P. 154 - 175
Published: Feb. 27, 2025
Introduction:
Neutrophils
are
key
players
in
the
hyperinflammatory
response
during
SARS-CoV-2
infection.
The
cytosolic
proliferating
cell
nuclear
antigen
(PCNA)
is
a
scaffolding
protein
highly
dependent
on
microenvironment
status
and
known
to
interact
with
numerous
proteins
that
regulate
neutrophil
functions.
This
study
aimed
examine
content
PCNA
interactome
neutrophils
from
COVID-19
patients.
Methods:
Proteomic
analyses
were
performed
cytosols
healthy
donors
patients
severe
or
critical
COVID-19.
In
vitro
approaches
used
explore
biological
significance
of
COVID-19-specific
interactome.
Results:
Neutrophil
cytosol
analysis
revealed
strong
interferon
(IFN)
signature,
variations
according
disease
severity.
Interactome
identified
associations
involved
signaling,
cytoskeletal
organization,
extracellular
trap
(NET)
formation,
such
as
arginine
deiminase
type-4
(PADI4)
histone
H3,
particularly
Functional
studies
signaling
showed
T2AA,
scaffold
inhibitor,
downregulated
IFN-related
genes,
including
STAT1,
MX1,
IFIT1,
IFIT2
neutrophils.
Additionally,
T2AA
specifically
inhibited
secretion
CXCL10,
an
IFN-dependent
cytokine.
was
also
found
effector
implicated
NET
especially
cases.
Conclusion:
has
unveiled
new
partners
enhance
pathway,
thereby
modulating
immune
responses
contributing
hyperinflammation
These
findings
provide
valuable
insights
into
dysregulation
other
immune-related
conditions.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 16, 2025
Chronic
inflammation
related
to
poor
genital
hygiene
is
a
well-recognized
pathogenic
trigger
for
penile
cancer
(PC).
The
neutrophil-to-lymphocyte
ratio
(NLR)
simple,
reproducible
systemic
inflammatory
marker
and
has
been
reported
indicate
unfavorable
outcomes.
However,
previous
studies
were
limited
by
small
sample
sizes,
confounding
prognostic
factors
lack
of
high-quality
evidence
demonstrating
the
significance
NLR
in
PC.
A
large
multicenter
cohort
582
PC
patients
who
underwent
radical
inguinal
lymphadenectomy
with
definitive
pN
stage
information
was
assessed.
Univariate
multivariate
Cox
regression
analyses
performed
investigate
value
inflammation-related
markers.
Propensity
score
matching
(PSM)
used
minimize
clinicopathological
features.
Immunofluorescence
assess
immunosuppressive
tumor
microenvironment
(TME).
high
preoperative
(≥
3.0)
associated
advanced
pT,
pN,
pathological
grade
lymphovascular
invasion
patients.
After
PSM
eliminate
interference
from
clinical
factors,
found
be
independent
indicators
(both
p<0.001).
NLRs
had
shorter
progression-free
survival
(PFS)
poorer
cisplatin-based
chemotherapy
PD-1
immunotherapy
response.
We
also
that
proinflammatory
cytokine
secretion
increased
N2
tumor-associated
neutrophils
(TANs)
infiltration
CD8+
T-cell
exhaustion
TME.
TANs
induced
neutrophil
extracellular
trap
formation
might
contribute
progression
resistance
high-NLR
an
effective,
simple
indicator
TME
Immunological Reviews,
Journal Year:
2022,
Volume and Issue:
314(1), P. 413 - 426
Published: Nov. 4, 2022
Summary
Neutrophils
are
the
most
abundant
innate
immune
cells
in
human
blood,
emerging
as
important
players
a
variety
of
diseases.
Mitochondria
bioenergetic,
biosynthetic,
and
signaling
organelles
critical
for
cell
fate
function.
have
been
overlooked
neutrophil
research
owing
to
conventional
view
that
neutrophils
contain
few,
if
any,
competent
mitochondria
do
not
rely
on
these
adenosine
triphosphate
production.
A
growing
body
evidence
suggests
participate
biology
at
many
levels,
ranging
from
development
chemotaxis,
effector
function,
death.
Moreover,
mitochondrial
components,
such
deoxyribonucleic
acid,
can
be
released
by
eliminate
infection
and/or
shape
response,
depending
specific
context.
In
this
review,
we
provide
an
update
functional
role
neutrophils,
highlight
key
modulating
phenotype
function
during
inflammation,
discuss
possibilities
challenges
exploit
unique
aspects
disease
treatment.
Journal of Immunology Research,
Journal Year:
2023,
Volume and Issue:
2023, P. 1 - 12
Published: Aug. 31, 2023
Systemic
lupus
erythematosus
(SLE)
is
a
complex
autoimmune
disease.
Approximately
one-third
to
two-thirds
of
the
patients
with
SLE
progress
nephritis
(LN).
The
pathogenesis
and
LN
has
not
yet
been
fully
elucidated,
effective
treatment
for
both
conditions
lacking.
endoplasmic
reticulum
(ER)
largest
intracellular
organelle
site
protein
synthesis,
lipid
metabolism,
calcium
storage.
Under
stress,
function
ER
disrupted,
accumulation
unfolded
or
misfolded
proteins
occurs
in
ER,
resulting
an
stress
(ERS)
response.
ERS
involved
dysfunction
B
cells,
macrophages,
T
dendritic
neutrophils,
other
immune
causing
system
disorders,
such
as
SLE.
In
addition,
also
renal
resident
cell
injury
contributes
progression
LN.
molecular
chaperones,
autophagy,
proteasome
degradation
pathways
inhibit
restore
homeostasis
improve
cells
injury.
This
may
be
therapeutic
strategy
this
review,
we
summarize
advances
field.
Biomedicines,
Journal Year:
2023,
Volume and Issue:
11(4), P. 1208 - 1208
Published: April 18, 2023
Uremia-induced
systemic
inflammation
is
partly
caused
by
the
dissemination
of
microbial
molecules
such
as
lipopolysaccharide
and
bacterial
double-stranded
DNA
from
leaked
gut
damaged
immune
cells
in
response
to
molecules.
Cyclic
GMP-AMP
synthase
(cGAS)
can
recognize
fragmented
induce
cGAMP
synthesis
for
activation
stimulator
interferon
genes
(STING)
pathway.
To
study
effect
cGAS
uremia-induced
inflammation,
we
performed
bilateral
nephrectomy
(BNx)
wild-type
knock-out
mice
found
that
leakage
blood
uremia
both
groups
were
similar.
However,
serum
cytokines
(TNF-α
IL-6)
neutrophil
extracellular
traps
(NETs)
decreased
significantly
cGAS-/-
neutrophils
after
stimulation
with
LPS
or
cell-free
DNA.
Transcriptomic
analysis
LPS-stimulated
also
confirmed
down-regulation
effector
functions.
The
flux
showed
exhibited
a
higher
respiratory
rate
than
despite
having
similar
mitochondrial
abundance
function.
Our
results
suggest
may
control
functions
respiration
Annals of Medicine,
Journal Year:
2024,
Volume and Issue:
56(1)
Published: Sept. 19, 2024
The
findings
of
the
last
decade
suggest
a
complex
link
between
inflammatory
cells,
coagulation,
and
activation
platelets
their
synergistic
interaction
to
promote
venous
thrombosis.
Inflammation
is
present
throughout
process
thrombosis,
various
metabolic
pathways
erythrocytes,
endothelial
immune
cells
involved
in
including
glucose
metabolism,
lipid
homocysteine
oxidative
stress,
are
associated
with
inflammation.
While
microenvironment
has
been
identified
as
marker
malignancy,
recent
studies
have
revealed
that
for
cancer
alterations
appear
also
be
potential
risk.
In
this
review,
we
discuss
how
synergy
metabolism
thrombosis
drives
thrombotic
disease.
We
explore
great
anti-inflammatory
strategies
targeting
anti-inflammation
metabolism.
Furthermore,
can
use
our
existing
knowledge
reduce
risk
Cells,
Journal Year:
2023,
Volume and Issue:
12(9), P. 1319 - 1319
Published: May 5, 2023
Type
1
diabetes
(T1D)
is
a
chronic
autoimmune
disease
characterized
by
T-cell-mediated
destruction
of
the
pancreatic
insulin-producing
beta
cells.
A
growing
body
evidence
suggests
that
abnormalities
in
neutrophils
and
neutrophil
extracellular
trap
(NET)
formation
(NETosis)
are
associated
with
T1D
pathophysiology.
However,
little
information
available
on
whether
these
changes
primary
defects
or
related
to
environmental
signals
encountered
during
active
disease.In
present
work,
NET
proteome
(NETome)
phorbol
12-myristate
13-acetate
(PMA)-
ionomycin-stimulated
from
people
established
compared
healthy
controls
(HC)
was
studied
proteomic
analysis.Levels
NETosis,
addition
plasma
levels
pro-inflammatory
cytokines
markers,
were
comparable
between
HC
subjects.
NETome
distinct
response
both
stimuli.
Quantitative
analysis
revealed
enriched
proteins
belonging
metabolic
pathways
(i.e.,
phosphoglycerate
kinase,
glyceraldehyde-3-phosphate
dehydrogenase,
UTP-glucose-1-phosphate
uridylyltransferase).
Complementary
profiling
rate
acidification,
an
approximate
measure
for
glycolysis,
mitochondrial
respiration
similar
stimuli.The
without
apparent
alteration
bio-energetic
profile
dysregulated
NETosis.
This
may
reflect
adaptation
mechanism
employed
activated
avoid
impaired
glycolysis
consequently
excessive
suboptimal
pivotal
innate
immune
defence
resolution
inflammation.
