Veterinary Sciences,
Год журнала:
2024,
Номер
11(11), С. 555 - 555
Опубликована: Ноя. 10, 2024
Influenza
A
virus
(IAV)
infection
initiates
a
complex
interplay
of
cell
death
modalities,
including
apoptosis,
necroptosis,
pyroptosis,
and
their
integration,
known
as
PANoptosis,
which
significantly
impacts
host
immune
responses
tissue
integrity.
These
pathways
are
intricately
regulated
by
viral
proteins
factors,
contributing
to
both
clearance
pathogenesis-related
damage.
This
review
comprehensively
explores
the
molecular
mechanisms
underlying
these
processes
in
influenza
infection.
We
highlight
roles
key
regulatory
proteins,
such
ZBP1
(Z-DNA
binding
protein
1)
RIPK3
(receptor-interacting
kinase
3),
orchestrating
responses,
emphasizing
dual
antiviral
defense
injury.
Furthermore,
we
discuss
emerging
therapeutic
strategies
targeting
pathways,
aiming
enhance
efficacy
while
minimizing
collateral
Future
research
should
focus
on
targeted
approaches
modulate
mechanisms,
reduce
damage
improve
clinical
outcomes
for
patients
with
severe
influenza.
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Июль 26, 2024
Idiopathic
pulmonary
fibrosis
(IPF)
is
a
lung
disease
that
worsens
over
time,
causing
in
the
lungs
and
ultimately
resulting
respiratory
failure
high
risk
of
death.
Macrophages
play
crucial
role
immune
system,
showing
flexibility
by
transforming
into
either
pro-inflammatory
(M1)
or
anti-inflammatory
(M2)
macrophages
when
exposed
to
different
stimuli,
impacting
development
IPF.
Recent
research
has
indicated
polarization
onset
progression
M1
secrete
inflammatory
cytokines
agents
early
damage
fibrosis,
while
M2
support
tissue
healing
releasing
cytokines.
Developing
novel
treatments
for
IPF
relies
on
thorough
comprehension
processes
involved
macrophage
The
review
outlines
regulation
its
impact
IPF,
with
goal
investigating
possible
therapeutic
benefits
advancement
The
endoplasmic
reticulum
(ER)
is
a
key
organelle
in
eukaryotic
cells,
responsible
for
wide
range
of
vital
functions,
including
the
modification,
folding,
and
trafficking
proteins,
as
well
biosynthesis
lipids
maintenance
intracellular
calcium
homeostasis.
A
variety
factors
can
disrupt
function
ER,
leading
to
aggregation
unfolded
misfolded
proteins
within
its
confines
induction
ER
stress.
conserved
cascade
signaling
events
known
protein
response
(UPR)
has
evolved
relieve
burden
restore
However,
these
processes
culminate
cell
death
while
stress
sustained
over
an
extended
period
at
elevated
levels.
This
review
summarizes
potential
role
UPR
determining
fate
various
diseases,
cardiovascular
neurodegenerative
metabolic
autoimmune
fibrotic
viral
infections,
cancer.
It
also
puts
forward
that
manipulation
this
intricate
pathway
may
represent
novel
target
drug
discovery
innovative
therapeutic
strategies
context
human
diseases.
International Immunopharmacology,
Год журнала:
2024,
Номер
140, С. 112768 - 112768
Опубликована: Июль 31, 2024
DNA
damage
is
typically
caused
during
cell
growth
by
replication
stress
or
exposure
to
endogenous
external
toxins.
The
accumulation
of
damaged
causes
genomic
instability,
which
the
root
cause
many
serious
disorders.
Multiple
cellular
organisms
utilize
sophisticated
signaling
pathways
against
damage,
collectively
known
as
response
(DDR)
networks.
Innate
immune
responses
are
activated
following
abnormalities,
including
damage.
Interestingly,
recent
studies
have
indicated
that
there
an
intimate
relationship
between
DDR
network
and
innate
responses.
Diverse
kinds
cytosolic
sensors,
such
cGAS
STING,
recognize
induce
signals
related
responses,
link
defective
immunity.
Moreover,
components
operate
in
IFNs
and/or
a
cascade
inflammatory
cytokines
via
direct
interactions
with
modulators.
Consistently,
factors
exacerbate
imbalance,
resulting
severe
diseases,
autoimmune
disorders
tumorigenesis.
Here,
latest
progress
understanding
crosstalk
reviewed.
Notably,
dual
function
modulators
may
provide
novel
insights
into
developing
targeted
immunotherapies
for
damage-related
even
carcinomas.
Cell Communication and Signaling,
Год журнала:
2024,
Номер
22(1)
Опубликована: Июль 23, 2024
Abstract
Many
DNA
viruses
develop
various
strategies
to
inhibit
cell
death
facilitate
their
replication.
However,
whether
influenza
A
virus
(IAV),
a
fast-replicating
RNA
virus,
attenuates
remains
unknown.
Here,
we
report
that
IAV
infection
induces
TAK1
phosphorylation
in
murine
alveolar
epithelial
line
(LET1)
and
fibroblastoma
(L929).
The
TAK1-specific
inhibitor
5Z-7-Oxzeneonal
(5Z)
knockout
significantly
enhance
IAV-induced
apoptosis,
as
evidenced
by
increased
PARP,
caspase-8,
caspase-3
cleavage.
inhibition
also
increases
necroptosis
RIPK1
S166
,
RIPK3
T231/S232
MLKL
S345
phosphorylation.
Mechanistically,
activates
IKK,
which
phosphorylates
S25
inhibits
its
activation.
p38
downstream
kinase
MK2,
S321
but
does
not
affect
Further
investigation
revealed
the
Nec-1
abrogate
apoptosis
necroptosis;
re-expression
of
wild-type
kinase-dead
(KD)-RIPK1
restores
death.
ZBP1
abrogates
death,
whereas
apoptosis.
5Z
treatment
enhances
slightly
reduces
inflammatory
response
lungs
H1N1
virus-infected
mice
prolongs
survival
IAV-infected
mice.
Our
study
provides
evidence
suppress
RIPK1-dependent
necroptosis,
is
required
for
cells.
Frontiers in Immunology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 6, 2025
Extracellular
vesicles
(EVs)
can
potently
inhibit
inflammation
yet
there
is
a
lack
of
understanding
about
the
impact
donor
characteristics
on
efficacy
EVs.
The
goal
this
study
was
to
determine
whether
sex
and
age
platelet-derived
EVs
(PEV)
affected
their
ability
viral
myocarditis.
PEV,
isolated
from
men
women
all
ages,
compared
PEV
obtained
under
50
years
age,
which
we
termed
premenopausal
(pmPEV).
Because
protective
effect
estrogen
against
myocardial
inflammation,
hypothesized
that
pmPEV
would
be
more
effective
than
at
inhibiting
We
injected
pmPEV,
or
vehicle
control
in
mouse
model
myocarditis
examined
histology,
gene
expression,
protein
profiles,
performed
proteome
microRNA
(miR)
sequencing
found
both
significantly
inhibited
myocarditis;
however,
effective,
confirmed
by
greater
reduction
inflammatory
cells
proinflammatory
profibrotic
markers
determined
using
expression
immunohistochemistry.
Proteome
miR
revealed
miRs
specifically
targeted
antiviral,
Toll-like
receptor
(TLR)4,
inflammasome
pathways
known
contribute
while
contained
general
immunoregulatory
miRs.
These
differences
EV
content
corresponded
differing
anti-inflammatory
effects
two
types
Frontiers in Microbiology,
Год журнала:
2025,
Номер
16
Опубликована: Фев. 5, 2025
Avian
reovirus
(ARV),
a
double-stranded
RNA
virus,
frequently
induces
immunosuppression
in
poultry,
leading
to
symptoms
such
as
irregular
bleeding
and
spleen
necrosis
infected
ducks.
Since
2017,
the
morbidity
mortality
rates
associated
with
ARV
infection
poultry
have
been
on
rise,
progressively
emerging
significant
viral
disease
impacting
duck
farming
industry
China.
In
our
study,
we
collected
embryo
fibroblasts
18
h
post-infection
conducted
transcriptome
sequencing
analysis.
The
analysis
revealed
that
3,818
mRNA
expressions
were
up-regulated,
4,573
down-regulated,
472
long
noncoding
RNAs
(LncRNAs)
345
lncRNAs
down-regulated.
We
employed
qRT-PCR
validate
results,
confirming
their
accuracy.
data
indicated
upregulation
of
PARP9
,
TLR7
TRIM33
ATG5
genes,
suggesting
potential
involvement
infection.
Notably,
study
identified
novel
functional
lncRNA,
MSTRG.9284.1
(It
was
named
linc000889
present
study),
which
inhibits
replication
at
transcriptional,
translational
levels
titer.
Overall,
this
has
numerous
ARV-induced
differentially
expressed
mRNAs
lncRNAs,
including
lncRNA
replication.
This
discovery
provides
new
insights
into
mechanisms
may
contribute
development
prevention
treatment
strategies.