Animals,
Journal Year:
2024,
Volume and Issue:
14(12), P. 1812 - 1812
Published: June 18, 2024
Mild–moderate
and
severe
equine
asthma
(MEA
SEA)
are
prevalent
inflammatory
airway
conditions
affecting
horses
of
numerous
breeds
disciplines.
Despite
extensive
research,
detailed
disease
pathophysiology
the
differences
between
MEA
SEA
still
not
completely
understood.
Bronchoalveolar
lavage
fluid
cytology,
broadly
used
in
clinical
practice
has
limited
means
to
represent
status
lower
airways.
Lipidomics
is
a
field
science
that
can
be
utilized
investigating
cellular
mechanisms
cell-to-cell
interactions.
Studies
lipidomics
have
broad
variety
foci,
which
fatty
acid
lipid
mediator
profile
analyses
global
been
implemented
veterinary
medicine.
As
many
crucial
proinflammatory
proresolving
mediators
lipids,
lipidomic
studies
offer
an
interesting
yet
largely
unexplored
investigate
reactions
The
aim
this
review
article
collect
summarize
findings
recent
on
inflammation.
Toxicological Sciences,
Journal Year:
2024,
Volume and Issue:
200(2), P. 324 - 345
Published: May 6, 2024
Constitutive
androstane
receptor
(CAR,
Nr1i3),
a
liver
nuclear
and
xenobiotic
sensor,
induces
drug,
steroid,
lipid
metabolizing
enzymes,
stimulates
hypertrophy
hyperplasia,
ultimately,
hepatocellular
carcinogenesis.
The
mechanisms
linking
early
CAR
responses
to
later
disease
development
are
poorly
understood.
Here
we
show
that
exposure
of
CD-1
mice
TCPOBOP
(1,4-bis[2-(3,5-dichloropyridyloxy)]benzene),
halogenated
xenochemical
selective
agonist
ligand,
pericentral
steatosis
marked
by
hepatic
accumulation
cholesterol
neutral
lipid,
elevated
circulating
alanine
aminotransferase,
indicating
hepatocyte
damage.
TCPOBOP-induced
was
weaker
in
the
region
but
stronger
periportal
females
compared
with
males.
Early
(1
day)
transcriptional
were
enriched
for
CAR-bound
primary
response
genes,
lipogenesis
metabolism
oxidative
stress
protection
pathways;
late
(2
weeks)
included
many
binding-independent
secondary
enrichment
macrophage
activation,
immune
response,
cytokine
reactive
oxygen
species
production.
Late
upstream
regulators
specific
TCPOBOP-exposed
male
linked
proinflammatory
carcinoma
progression.
administered
weekly
using
high
corn
oil
vehicle
induced
carbohydrate-responsive
transcription
factor
(MLXIPL)-regulated
target
dysregulated
mitochondrial
respiratory
translation
regulatory
pathways,
more
advanced
pathology.
Overall,
recapitulates
histological
gene
expression
changes
characteristic
emerging
steatotic
disease,
including
nonparenchymal
cells
indicative
transition
state.
Upstream
both
genes
include
novel
biomarkers
foreign
chemical-induced
metabolic
dysfunction-associated
disease.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Feb. 20, 2024
Abstract
Constitutive
Androstane
Receptor
(CAR,
Nr1i3
),
a
liver
nuclear
receptor
and
xenobiotic
sensor,
induces
drug,
steroid
lipid
metabolizing
enzymes,
stimulates
hypertrophy
hyperplasia,
ultimately,
hepatocellular
carcinogenesis.
The
mechanisms
linking
early
CAR
responses
to
subsequent
disease
development
are
poorly
understood.
Here
we
show
that
exposure
of
CD-1
mice
TCPOBOP,
halogenated
xenochemical
selective
agonist
ligand,
pericentral
steatosis
marked
by
hepatic
accumulation
cholesterol
neutral
lipid,
elevated
circulating
alanine
aminotransferase
levels,
indicating
hepatocyte
damage.
TCPOBOP-induced
was
weaker
in
the
region
but
stronger
periportal
females
compared
males.
Early
(1-day)
TCPOBOP
transcriptional
were
enriched
for
CAR-bound
primary
response
genes,
metabolism
oxidative
stress
protection
pathways;
late
(2-wk)
included
many
binding-independent
secondary
with
enrichment
immune
response,
macrophage
activation,
cytokine
reactive
oxygen
species
production.
Late
upstream
regulators
specific
TCPOBOP-exposed
male
linked
pro-inflammatory
carcinoma
progression.
administered
weekly
using
high
corn
oil
vehicle
activated
carbohydrate-responsive
transcription
factor
(MLXIPL)-regulated
target
dysregulated
mitochondrial
respiratory
translation
regulatory
pathways,
induced
more
advanced
pathology.
Thus,
recapitulates
histological
gene
expression
changes
characteristic
emerging
steatotic
disease,
including
non-parenchymal
cells
indicative
transition
state.
Upstream
both
include
novel
biomarkers
foreign
chemical-induced
metabolic
dysfunction-associated
disease.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: July 23, 2024
Abstract
Mycobacterium
tuberculosis
(
Mtb
)
infection
of
macrophages
reprograms
cellular
metabolism
to
promote
lipid
retention.
While
it
is
clearly
known
that
intracellular
utilize
host
derived
lipids
maintain
infection,
the
role
macrophage
processing
on
bacteria’s
ability
access
pool
remains
undefined.
We
utilized
a
CRISPR-Cas9
genetic
approach
assess
impact
sequential
steps
in
fatty
acid
growth
.
Our
analyzes
demonstrate
which
cannot
either
import,
store
or
catabolize
acids
restrict
by
both
common
and
divergent
anti-microbial
mechanisms,
including
increased
glycolysis,
oxidative
stress,
production
pro-inflammatory
cytokines,
enhanced
autophagy
nutrient
limitation.
also
show
impaired
droplet
biogenesis
restrictive
replication,
but
induction
same
fails
rescue
growth.
work
expands
our
understanding
how
homeostasis
impacts
macrophage.
Glia,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 17, 2024
Lipids
are
small
molecule
immunomodulators
that
play
critical
roles
in
maintaining
cellular
health
and
function.
Microglia,
the
resident
immune
cells
of
central
nervous
system,
regulate
lipid
metabolism
both
extracellular
environment
within
intracellular
compartments
through
various
mechanisms.
For
instance,
glycerophospholipids
fatty
acids
interact
with
protein
receptors
on
microglial
surface,
such
as
Triggering
Receptor
Expressed
Myeloid
Cells
2,
influencing
functions
like
phagocytosis
migration.
Moreover,
cholesterol
is
essential
not
only
for
survival
but,
along
other
lipids
acids,
crucial
formation,
function,
accumulation
droplets,
which
modulate
activity
inflammatory
diseases.
Other
lipids,
including
acylcarnitines
ceramides,
participate
signaling
pathways
microglia.
Despite
complexity
lipidome,
a
few
studies
have
investigated
effects
specific
classes
biology.
In
this
review,
we
focus
major
their
modulating
We
also
discuss
novel
analytical
techniques
characterizing
lipidome
highlight
gaps
current
knowledge,
suggesting
new
directions
future
research
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Feb. 28, 2024
Summary
Acute
infection
of
the
central
nervous
system
is
one
deadliest
diseases,
but
mechanisms
by
which
intracellular
bacteria
infiltrate
brain
remain
poorly
understood.
Phagocytic
cells
are
usually
recognized
as
battlefield
on
war
waged
against
bacteria;
however,
little
known
about
how
take
advantage
infected
phagocytes
to
access
brain.
In
this
study,
we
find
that
a
novel
CD36
+
Fabp4
Pparg
macrophage
subpopulation
(CD36
macrophage)
participates
in
penetration
without
disruption
brain-blood
barrier.
Biomechanical
analysis
reveals
abundant
protrusions
and
adhesion
molecules
macrophages
confer
significant
resistance
mechanical
stress
blood
flow,
thereby
providing
more
opportunities
for
these
adhere
vascular
endothelial
surface.
Through
metabolomics
analysis,
lipid
metabolism
dysregulated
during
bacterial
neuroinvasion,
β-hydroxybutyrate
promotes
formation
survival
macrophages.
Importantly,
ketogenesis
exacerbates
symptoms
could
be
alleviated
supplementing
with
physiological
level
glucose.
Taken
together,
our
findings
uncover
pathway
hijack
invade
brain,
suggesting
might
play
role
prevention
or
resolution
neuroinvasion.
Graphic
Abstract
Emergency and Critical Care Medicine,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Aug. 6, 2024
Abstract
As
one
of
the
pathological
causes
coronary
heart
disease,
atherosclerosis
poses
a
major
threat
to
human
health.
Macrophages
play
an
important
role
in
regulating
atherosclerotic
disease
progression.
Specifically,
inflammation
is
initiated
when
low-density
lipoproteins
infiltrate
subcutaneous
area
and
are
phagocytosed
by
macrophages,
leading
foam
cell
formation.
The
subsequent
progression
or
resolution
depends
on
delicate
balance
between
proinflammatory
anti-inflammatory
mediators.
In
cases
where
factors
dominate,
macrophages
tend
activate
pyroptosis
necrosis
pathways,
resulting
release
intracellular
damage-associated
molecular
patterns
promoting
necrotic
core
formation
plaque
Conversely,
prevail,
engage
autophagy-mediated
lipid
metabolism
while
inhibiting
through
efferocytosis
apoptotic
cells.
regulatory
function
can
also
be
understood
from
perspective
their
life
cycles.
Lipid
retention
within
arterial
intima
its
uptake
characteristic
hallmarks
atherosclerosis.
pivotal
effector
cells
this
process,
with
distinctive
performances
decisively
determine
inflammation.
complete
cycle
plaques
encompasses
chemotaxis,
infiltration,
polarization,
for
metabolic
efflux,
formation,
overload,
various
forms
programmed
necrosis,
including
autophagy,
pyroptosis,
apoptosis,
efferocytosis,
facilitate
removal
limit
behavior
has
rarely
been
comprehensively
addressed
previous
review
articles.
This
article
provides
extensive
overview
entire
following
response
impact
resolution.
Considering
that
inflammatory
associated
atherosclerosis,
targeting
regulation
holds
promise
therapeutic
interventions
against
atherosclerosis-related
cardiovascular
diseases.