Alteration in Tracheal Morphology and Transcriptomic Features in Calves After Infection with Mycoplasma bovis
Fan Liu,
No information about this author
Fei Yang,
No information about this author
Lei Guo
No information about this author
et al.
Microorganisms,
Journal Year:
2025,
Volume and Issue:
13(2), P. 442 - 442
Published: Feb. 18, 2025
Mycoplasma
bovis
is
one
of
the
most
important
pathogens
in
animal
husbandry,
and
current
infection
morbidity
rates
are
increasing
year
by
year,
causing
great
losses
to
farming
industry
seriously
affecting
welfare.
In
this
study,
we
took
tracheal
tissues
from
calves
infected
with
M.
make
pathological
tissue
sections
for
observation,
selected
transcriptome
sequencing
screen
differentially
expressed
genes
based
on
threshold
|log2FoldChange|
>
1
Padjust
<
0.05
functional
enrichment,
explore
depth
potential
mechanisms
bovine
damage
caused
tracheitis.
Experiments
were
conducted
observe
changes
after
through
trachea
bovis-infected
calves.
From
results,
mined
main
differential
metabolic
pathways
It
was
found
that
cricoid
cartilage
congested
hemorrhagic
calves,
showed
localized
necrosis
epithelial
cells,
disorganization,
high
inflammatory
cell
infiltration
interepithelial
lamina
propria,
some
detachment.
Transcriptome
identified
4199
DEGs,
including
1378
up-regulated
2821
down-regulated
genes.
KEGG
enrichment
analysis
indicated
enriched
59
significantly
differing
signaling
pathways,
a
number
related
tracheitis
induced
unearthed.
The
major
ones
included
IL-17,
Toll-like
receptor,
JAK/STAT,
PI3K-Akt
pathway,
etc.
trachea,
results
also
significant
differences
expression
key
such
as
IL-6
factor,
CASP8,
APOA1.
Language: Английский
Exploring Ferroptosis in Allergic Inflammatory Diseases: Emerging Mechanisms and Therapeutic Perspectives
Henry Sutanto,
No information about this author
Laras Pratiwi,
No information about this author
Deasy Fetarayani
No information about this author
et al.
Cell Biology International,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 22, 2025
ABSTRACT
Ferroptosis,
a
unique
form
of
regulated
cell
death
driven
by
iron
accumulation
and
lipid
peroxidation,
has
emerged
as
critical
process
in
various
diseases.
Recent
evidence
suggests
its
involvement
the
pathogenesis
allergic
diseases,
including
asthma,
rhinitis,
atopic
dermatitis.
These
conditions
are
characterized
chronic
inflammation,
oxidative
stress,
immune
dysregulation,
all
which
intersect
with
molecular
mechanisms
ferroptosis.
Key
regulators,
such
glutathione
peroxidase
4
(GPX4),
cystine/glutamate
antiporter
system
Xc‐,
metabolism
pathways,
play
pivotal
roles
ferroptotic
processes
their
contribution
to
disease
progression.
This
review
explores
mechanistic
link
between
ferroptosis
emphasizing
how
damage
overload
exacerbate
inflammation
tissue
injury.
We
also
highlight
emerging
diagnostic
biomarkers,
peroxidation
products
could
improve
monitoring
stratification.
Therapeutic
strategies
targeting
ferroptosis,
GPX4
activators,
chelators,
inhibitors,
show
promise
preclinical\
studies,
offering
potential
new
avenues
for
treating
However,
challenges
remain
translating
these
findings
into
clinical
applications.
By
integrating
current
knowledge,
this
underscores
need
further
research
both
biomarker
therapeutic
target
Language: Английский