Thetreatment
of
infected
wounds
is
currently
a
major
challenge
in
clinical
medicine,
and
enhancing
antimicrobial
angiogenic
capacity
one
the
most
common
strategies.
However,
current
treatment
makes
it
difficult
to
balance
effect
early
stage
later
stages
wound
healing,
leading
an
increased
rate
poor
prognosis.
Here,
we
present
nanoconductive
hydrogel
EF@S-HGM,
consisting
HGM
with
ECGS,
FMLP,
SWCNT.
The
host-guest
supramolecular
macromolecule
(HGM)
biocompatible
can
be
injected
situ
wound.
endothelial
cell
growth
factor
(ECGS)
accelerates
vascular
remodeling
repairs
by
promoting
proliferation
cells.
N-Formyl-Met-Leu-Phe
(FMLP)
recruits
neutrophils
increases
capacity.
Single-walled
carbon
nanotubes
(SWCNT)
make
conductive,
enabling
utilize
endogenous
electric
field
recruit
multiple
kinds
In
addition,
found
that
EF@S-HGM
activates
glucocorticoid
receptor
senescence
pathway
promotes
formation
NET,
which
enhances
effect.
As
tissue-engineered
skin,
conductive
promising
material
for
regenerative
medicine
may
provide
potential
option
care
significantly
improve
patient
outcomes
Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Март 18, 2024
Abstract
Background
Retinal
degeneration
results
from
disruptions
in
retinal
homeostasis
due
to
injury,
disease,
or
aging
and
triggers
peripheral
leukocyte
infiltration.
Effective
immune
responses
rely
on
coordinated
actions
of
resident
microglia
recruited
macrophages,
critical
for
tissue
remodeling
repair.
However,
these
phagocytes
also
contribute
chronic
inflammation
degenerated
retinas,
yet
the
precise
coordination
response
damage
remains
elusive.
Recent
investigations
have
demonstrated
that
phagocytic
cells
can
produce
extracellular
traps
(ETs),
which
are
a
source
self-antigens
alter
response,
potentially
lead
injury.
Methods
Innovations
experimental
systems
facilitate
real-time
exploration
cell
interactions
dynamic
responses.
We
integrated
vivo
imaging
with
ultrastructural
analysis,
transcriptomics,
pharmacological
treatments,
knockout
mice
elucidate
role
their
modulation
local
inflammatory
through
(ETs).
Deciphering
mechanisms
is
essential
developing
novel
enhanced
immunotherapeutic
approaches
redirect
specific
maladaptive
towards
favorable
wound
healing
retina.
Results
Our
findings
underscore
pivotal
innate
cells,
especially
macrophages/monocytes,
regulating
repair
inflammation.
The
absence
neutrophil
macrophage
infiltration
aids
parenchymal
integrity
restoration,
while
depletion,
particularly
impedes
vascular
recovery.
demonstrate
when
retina,
release
chromatin
granular
proteins,
forming
ETs.
Furthermore,
inhibition
ETosis
support
repair,
surpassing
effects
blocking
recruitment.
Simultaneously,
reshapes
causing
neutrophils,
helper,
cytotoxic
T-cells
be
restricted
primarily
superficial
capillary
plexus
instead
reaching
damaged
photoreceptor
layer.
Conclusions
data
offer
insights
into
immunity's
responding
help
innovative
shift
beneficial
regeneration.
ACS Infectious Diseases,
Год журнала:
2025,
Номер
11(2), С. 483 - 492
Опубликована: Янв. 31, 2025
Neutrophils,
the
first
cells
to
arrive
at
infection
sites,
release
neutrophil
extracellular
traps
(NETs)
comprising
nuclear
and/or
mitochondrial
DNA
webs
decorated
with
proteins.
Similar
other
parasites,
Leishmania
infantum
induces
NET
extrusion.
However,
our
understanding
of
formation
and
fate
after
in
a
context
is
limited.
Our
study
aimed
determine
origin
scaffolds
released
by
human
neutrophils
response
chemical
or
L.
stimulation.
Neutrophils
were
incubated
PMA,
PHA,
LPS,
infantum,
followed
elastase
activity
quantification;
additionally,
we
evaluated
source
that
composes
NETs.
Neutrophil
viability
was
annexin-V/7AAd
labeling.
Expression
IL6,
TNFA,
IL10,
CXCL1,
CXCL8,
FPR1
interaction
assessed.
chemicals
stimulated
showed
lower
1
h
comparison
parasites.
NETs
from
chemically
mainly
composed
DNA.
Conversely,
induced
parasites
had
no
leishmanicidal
activity.
After
4
parasite
stimulation,
peak
expression
genes
such
as
FPR1.
demonstrates
produce
exposure.
Although
they
are
not
toxic
parasite,
danger
signals.
These
findings
support
role
releasing
signaling
molecules,
which
influence
inflammatory
environment
infectious
process
occurs.
Current Issues in Molecular Biology,
Год журнала:
2025,
Номер
47(2), С. 133 - 133
Опубликована: Фев. 19, 2025
Cellular
nucleosomes-the
structural
and
functional
units
of
chromatin-are
inherently
present
in
cells.
During
cellular
damage
or
cell
death,
nucleosomes
are
released
into
circulation,
either
actively
passively.
Once
released,
can
become
immunogenic
entities
through
various
mechanisms.
The
nucleosomal
proteins
nucleosomes,
called
histones,
play
a
pivotal
role
inducing
immunogenicity.
However,
intact
more
than
the
histones
alone,
as
double-stranded
deoxyribonucleic
acid
(dsDNA)
enhances
its
potential.
Our
recent
study
has
shown
that
circulating
predominantly
rather
free
histones.
Consequently,
primarily
function
integral
parts
acting
independently.
Circulating
their
associated
implicated
pathogenesis
wide
array
diseases.
Notably,
they
critical
lung
injury
sepsis.
These
diseases
have
high
morbidity
mortality
rates
lack
early
diagnostic
biomarkers.
Further
investigation
is
required
to
fully
elucidate
disease
processes.
This
review
aims
discuss
current
understanding
sepsis,
with
focus
on
underlying
Journal of Innate Immunity,
Год журнала:
2025,
Номер
17(1), С. 154 - 175
Опубликована: Фев. 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.
