Critical Reviews in Microbiology,
Год журнала:
2024,
Номер
unknown, С. 1 - 21
Опубликована: Июнь 25, 2024
Mycobacterium
tuberculosis
(Mtb)
is
the
causative
pathogen
of
tuberculosis,
most
lethal
infectious
disease
resulting
in
1.3
million
deaths
annually.
Treatments
against
Mtb
are
increasingly
impaired
by
growing
prevalence
antimicrobial
drug
resistance,
which
necessitates
development
new
antibiotics
or
alternative
therapeutic
approaches.
Upon
infecting
host
cells,
predominantly
macrophages,
becomes
critically
dependent
on
lipids
as
a
source
nutrients.
Additionally,
produces
numerous
lipid-based
virulence
factors
that
contribute
to
pathogen's
ability
interfere
with
host's
immune
responses
and
create
lipid
rich
environment
for
itself.
As
lipids,
metabolism
manipulating
play
an
important
role
Mtb,
this
review
provides
state-of-the-art
overview
mycobacterial
concomitant
host-pathogen
interaction
therein.
While
doing
so,
we
will
emphasize
unexploited
bacteria-directed
host-directed
targets,
highlight
potential
synergistic
combinations
hold
promise
interventions.
Acute
lung
injury
(ALI)
and
acute
respiratory
distress
syndrome
(ARDS)
are
the
result
of
an
exaggerated
inflammatory
response
triggered
by
a
variety
pulmonary
systemic
insults.
The
tissues
comprised
cell
types,
including
alveolar
epithelial
cells,
vascular
endothelial
macrophages,
neutrophils,
others.
There
is
mounting
evidence
that
these
diverse
populations
within
interact
to
regulate
inflammation
in
both
direct
indirect
stimuli.
aim
this
review
provide
summary
discussion
recent
advances
understanding
importance
cell-cell
crosstalk
pathogenesis
ALI/ARDS,
with
specific
focus
on
interactions
may
offer
prospective
therapeutic
avenues
for
ALI/ARDS.
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 8, 2025
To
investigate
the
mechanisms
behind
worsening
of
acute
lung
injury
(ALI)
in
obesity,
transcriptomic
sequencing
is
performed,
and
significantly
reduced
mRNA
levels
Aconitate
Decarboxylase
1
(ACOD1)
tissue
high-fat
diet
(HFD)
mice
are
found.
Clinical
samples
collected,
an
ALI
model
established
HFD
mice,
both
human
mouse
analyzed,
revealing
a
significant
decrease
ACOD1
expression
alveolar
macrophages
obesity.
Further
vivo
vitro
experiments
show
that
knockdown
worsens
injury,
inflammation,
oxidative
stress,
while
overexpression
alleviates
these
effects.
Moreover,
nuclear
factor
erythroid
2-related
2
(Nrf2)
inhibition
diminishes
protective
effects
exacerbated
by
Additionally,
context
growth
independent
(GFI1)
protein
elevated
macrophages,
its
leads
to
upregulated
expression.
Therefore,
this
study
suggests
downregulation
key
likely
driven
GFI1
upregulation.
Respiratory Research,
Год журнала:
2024,
Номер
25(1)
Опубликована: Март 30, 2024
Abstract
Inflammation
and
immune
processes
underlie
pulmonary
hypertension
progression.
Two
main
different
activated
phenotypes
of
macrophages,
classically
M1
macrophages
alternatively
M2
are
both
involved
in
inflammatory
related
to
hypertension.
Recent
advances
suggest
that
coordinate
interactions
among
proinflammatory
anti-inflammatory
mediators,
other
cellular
components
such
as
smooth
muscle
cells
fibroblasts.
In
this
review,
we
summarize
the
current
literature
on
role
pathogenesis
hypertension,
including
origin
their
response
triggers
We
then
discuss
cytokines,
vascular
adventitial
fibroblasts
well
potential
therapeutic
benefits
disease.
Identifying
critical
will
contribute
a
comprehensive
understanding
pathophysiological
abnormality,
may
provide
new
perspectives
for
management.
Ecotoxicology and Environmental Safety,
Год журнала:
2024,
Номер
284, С. 116899 - 116899
Опубликована: Авг. 23, 2024
Silicosis
is
a
lethal
occupational
disease
caused
by
long-term
exposure
to
respirable
silica
dust.
Pulmonary
macrophages
play
crucial
role
in
mediating
the
initiation
of
silicosis.
However,
phenotypic
and
functional
heterogeneities
pulmonary
silicosis
have
not
been
well-studied.