Abstract
Background
Inflammatory
and
immune
responses
in
the
brain
that
contribute
to
various
neuropsychiatric
disorders
may
begin
as
microglial
“priming”.
Interferon
(IFN)‐γ
is
known
cause
priming,
but
mechanism
unclear.
Methods
We
examined
effects
of
IFN‐γ
on
gene
expression,
activation,
inflammatory
activity
NLRP3
inflammasome
primary
microglia
brains
mice.
Results
Our
results
showed
treating
cultures
with
induced
a
hedgehog‐like
morphology
upregulated
markers
activation
(CD86,
CD11b)
pro‐inflammatory
molecules
(IL‐1β,
IL‐6,
TNF‐α,
iNOS),
while
downregulating
homeostasis
(CX3CR1,
CD200R1),
anti‐inflammatory
(MCR1,
Arg‐1)
neurotrophic
factors
(IGF‐1,
BDNF).
also
(NLRP3,
caspase‐1,
gasdermin
D,
IL‐18).
This
particular
transcriptional
profiling
makes
IFN‐γ‐primed
exaggerated
upon
lipopolysaccharide
(LPS)
stimulation.
The
level
NLRP3,
IL‐1β,
IL‐18,
TNF‐α
iNOS
treated
both
LPS
were
highest
than
either
one
alone.
Injecting
into
lateral
ventricle
mice
similar
morphological
functional
changes
hippocampal
cultures.
from
or
hippocampus
abolished
when
STAT1
was
inhibited
using
fludarabin.
alone
together
anxiety‐
depression‐like
behaviors
impaired
hippocampus‐dependent
spatial
memory;
these
mitigated
by
Conclusions
primes
activating
STAT1,
which
upregulates
genes
activate
inflammasome.
Inhibiting
IFN‐γ/STAT1
axis
be
way
treat
neurodegenerative
diseases
psychiatric
involve
priming.
Neurology International,
Journal Year:
2025,
Volume and Issue:
17(4), P. 47 - 47
Published: March 24, 2025
Background:
Chronic
aberrant
inflammation
is
a
crucial
step
in
mediating
cerebrovascular
and
neurodegenerative
pathologies,
including
Alzheimer’s
Parkinson’s
disease.
Due
to
their
exceptional
antioxidant
properties
ability
alter
imbalance
metabolism
reactive
response,
cocoa-derived
flavanols
are
being
investigated
as
potential
bioactive
substances
modulate
reverse
these
inflammation-associated
disorders.
Objective:
The
present
study
will
focus
on
the
possible
beneficial
effects
of
extract,
enhanced
with
other
phytochemicals
such
spirulina
pineapple,
selected
biomarkers
inflammatory,
metabolic,
processes.
Methods:
A
mice
model
was
treated
extract
cocktail,
biomolecular
data
obtained
by
performing
immunohistochemical
biochemical
analysis.
Results:
Results
show
that
mitigates
neuroinflammatory
processes
triggered
(decreased
expression
macrophage
CD11b)
prevents
escalade
subsequent
neurodegeneration
pathologies.
Conclusions:
results
based
hypo-vitaminosis,
neuroinflammation,
inmunoreactive
analysis
suggest
powerful
bioproduct
for
ameliorating
mediate
metabolic
diseases.
BMC Medicine,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: April 30, 2025
Epidemiological
studies
that
have
simultaneously
explored
the
effects
of
placental
and
cord
blood
inflammatory
cytokine
levels
on
neurodevelopment
in
offspring,
as
well
role
maternal
vitamin
D
these
associations,
are
lacking.
To
investigate
associations
with
18-month-old
children,
potential
modification
effect
by
D.
Based
Ma'anshan
birth
cohort,
current
study
involved
1241
mother-child
pairs.
The
mRNA
expression
levels,
serum
concentrations,
concentrations
were
determined.
Children's
neurodevelopmental
outcomes
defined
Chinese
version
Ages
Stages
Questionnaire
(Third
Edition)
subdomain
scores
below
established
cutoff
scores.
Generalized
linear
models
utilized
to
assess
cytokines
examine
After
adjusting
for
confounders,
each
one-unit
increase
IL-6
(OR
=
1.30,
95%
CI:
1.09,
1.55,
P-FDR
0.024),
IL-8
1.25,
1.05,
1.49,
0.036),
IFN-γ
level
1.74,
1.16,
2.61,
0.042)
was
associated
an
increased
risk
fine
motor
delay.
Elevated
TNF-α
1.38,
1.12,
1.69,
0.012),
1.29,
1.04,
1.61,
0.042),
1.31,
1.06,
1.62,
0.036)
personal-social
Stratified
analyses
showed
lower
(<
20
ng/mL)
moderated
between
markers
delays
motor,
gross
subdomains.
specific
placenta
umbilical
developmental
a
parental-reported
screening
tool.
Maternal
status
can
modify
adverse
intrauterine
pro-inflammatory
milieu
children.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 4, 2024
Organ
transplantation
is
the
gold
standard
therapy
for
end-stage
organ
failure.
However,
shortage
of
available
grafts
and
long-term
graft
dysfunction
remain
primary
barriers
to
transplantation.
Exploring
approaches
solve
these
issues
urgent,
CRISPR/Cas9-based
transcriptome
editing
provides
one
potential
solution.
Furthermore,
combining
gene
with
an
ex
vivo
perfusion
system
would
enable
pre-implantation
grafts.
How
determine
effective
intervention
targets
becomes
a
new
problem.
Fortunately,
advent
high-throughput
CRISPR
screening
has
dramatically
accelerated
targets.
This
review
summarizes
current
advancements,
utilization,
workflow
in
various
immune
non-immune
cells.
It
also
discusses
ongoing
applications
CRISPR/Cas-based
prospective
solid
Cellular and Molecular Life Sciences,
Journal Year:
2024,
Volume and Issue:
81(1)
Published: Aug. 17, 2024
Parkinson's
disease
(PD)
is
the
second
most
common
neurodegenerative
disease,
and
its
hallmark
pathological
features
are
loss
of
dopaminergic
(DA)
neurons
in
midbrain
substantia
nigra
pars
compacta
(SNpc)
accumulation
alpha-synuclein
(α-syn).
It
has
been
shown
that
integrity
blood-brain
barrier
(BBB)
damaged
PD
patients,
a
large
number
infiltrating
T
cells
inflammatory
cytokines
have
detected
cerebrospinal
fluid
(CSF)
brain
parenchyma
patients
animal
models,
including
significant
change
proportion
different
CD4
Abstract
Background
Inflammatory
and
immune
responses
in
the
brain
that
contribute
to
various
neuropsychiatric
disorders
may
begin
as
microglial
“priming”.
Interferon
(IFN)‐γ
is
known
cause
priming,
but
mechanism
unclear.
Methods
We
examined
effects
of
IFN‐γ
on
gene
expression,
activation,
inflammatory
activity
NLRP3
inflammasome
primary
microglia
brains
mice.
Results
Our
results
showed
treating
cultures
with
induced
a
hedgehog‐like
morphology
upregulated
markers
activation
(CD86,
CD11b)
pro‐inflammatory
molecules
(IL‐1β,
IL‐6,
TNF‐α,
iNOS),
while
downregulating
homeostasis
(CX3CR1,
CD200R1),
anti‐inflammatory
(MCR1,
Arg‐1)
neurotrophic
factors
(IGF‐1,
BDNF).
also
(NLRP3,
caspase‐1,
gasdermin
D,
IL‐18).
This
particular
transcriptional
profiling
makes
IFN‐γ‐primed
exaggerated
upon
lipopolysaccharide
(LPS)
stimulation.
The
level
NLRP3,
IL‐1β,
IL‐18,
TNF‐α
iNOS
treated
both
LPS
were
highest
than
either
one
alone.
Injecting
into
lateral
ventricle
mice
similar
morphological
functional
changes
hippocampal
cultures.
from
or
hippocampus
abolished
when
STAT1
was
inhibited
using
fludarabin.
alone
together
anxiety‐
depression‐like
behaviors
impaired
hippocampus‐dependent
spatial
memory;
these
mitigated
by
Conclusions
primes
activating
STAT1,
which
upregulates
genes
activate
inflammasome.
Inhibiting
IFN‐γ/STAT1
axis
be
way
treat
neurodegenerative
diseases
psychiatric
involve
priming.