Frontiers in Immunology,
Год журнала:
2022,
Номер
13
Опубликована: Окт. 6, 2022
As
the
essential
regulators
of
organ
fibrosis,
macrophages
undergo
marked
phenotypic
and
functional
changes
after
injury.
These
in
macrophage
phenotype
function
can
result
maladaptive
repair,
causing
chronic
inflammation
development
pathological
fibrosis.
Autophagy,
a
highly
conserved
lysosomal
degradation
pathway,
is
one
major
players
to
maintain
homeostasis
through
clearing
protein
aggregates,
damaged
organelles,
invading
pathogens.
Emerging
evidence
has
shown
that
autophagy
plays
an
role
polarization,
inflammation,
Because
high
heterogeneity
different
organs,
types
may
play
roles
Here,
we
review
current
understanding
fibrosis
highlight
potential
treatment
Finally,
important
unresolved
issues
this
field
are
briefly
discussed.
A
better
mechanisms
contribute
developing
novel
therapies
for
inflammatory
diseases
Abstract
Lung
tissue
has
a
certain
regenerative
ability
and
triggers
repair
procedures
after
injury.
Under
controllable
conditions,
lung
can
restore
normal
structure
function.
Disruptions
in
this
process
lead
to
respiratory
system
failure
even
death,
causing
substantial
medical
burden.
The
main
types
of
diseases
are
chronic
obstructive
pulmonary
disease
(COPD),
idiopathic
fibrosis
(IPF),
acute
distress
syndrome
(ARDS).
Multiple
cells,
such
as
epithelial
endothelial
fibroblasts,
immune
involved
regulating
the
Although
mechanism
that
regulates
not
been
fully
elucidated,
clinical
trials
targeting
different
cells
signaling
pathways
have
achieved
some
therapeutic
effects
diseases.
In
review,
we
provide
an
overview
cell
type
regeneration
repair,
research
models,
summarize
molecular
mechanisms
regulation
fibrosis.
Moreover,
discuss
current
stem
therapy
pharmacological
strategies
for
COPD,
IPF,
ARDS
treatment.
This
review
provides
reference
further
on
cellular
regeneration,
drug
development,
trials.
Frontiers in Immunology,
Год журнала:
2022,
Номер
13
Опубликована: Июнь 29, 2022
Drinking
alcohol,
even
in
moderation,
can
affect
the
immune
system.
Studies
have
shown
disproportionate
effects
of
alcohol
on
circulating
and
tissue-resident
myeloid
cells
(granulocytes,
monocytes,
macrophages,
dendritic
cells).
These
orchestrate
body's
first
line
defense
against
microbial
challenges
as
well
maintain
tissue
homeostasis
repair.
Alcohol's
these
are
dependent
exposure
pattern,
with
acute
drinking
dampening
but
chronic
enhancing
production
inflammatory
mediators.
Although
is
associated
heightened
systemic
inflammation,
studies
resident
macrophage
populations
several
organs
including
spleen,
liver,
brain,
lung
also
compromised
functional
metabolic
capacities
cells.
Many
thought
to
be
mediated
by
oxidative
stress
caused
its
metabolites
which
directly
impact
cellular
epigenetic
landscapes.
In
addition,
since
relatively
short-lived
circulation
under
constant
repopulation
from
bone
marrow
compartment,
alcohol's
progenitors
hematopoiesis
important
for
understanding
systemically
populations.
Alcohol-induced
disruption
progenitor,
circulating,
contribute
increased
susceptibility
patients
use
disorders
viral
bacterial
infections.
this
review,
we
provide
an
overview
consumption
function
monocytes
macrophages
host
defense,
repair
inflammation.
We
then
summarize
our
current
mechanisms
underlying
alcohol-induced
examine
changes
transcriptome
epigenome
mcrophages.
Overall,
leads
hyper-inflammation
concomitant
decreased
wound
healing
responses
monocytes/macrophages
due
a
rewiring
epigentic
transcriptional
landscape.
However,
advanced
alcoholic
liver
disease,
become
immunosuppressed
response
surrounding
hyper-inflammatory
milieu.
Therefore,
effect
depends
disease
state
cell
population.
Dysfunction
of
alveolar
epithelial
type
2
cells
(AEC2s),
the
facultative
progenitors
lung
alveoli,
is
implicated
in
pulmonary
disease
pathogenesis,
highlighting
importance
human
vitro
models.
However,
AEC2-like
culture
have
yet
to
be
directly
compared
their
vivo
counterparts
at
single-cell
resolution.
Here,
we
performed
head-to-head
comparisons
among
transcriptomes
primary
(1°)
adult
AEC2s,
cultured
progeny,
and
induced
pluripotent
stem
cell–derived
AEC2s
(iAEC2s).
We
found
each
population
occupied
a
distinct
transcriptomic
space
with
(1°
iAEC2s)
exhibiting
similarities
differences
from
freshly
purified
1°
cells.
Across
cell
type,
an
inverse
relationship
between
proliferative
maturation
states,
preculture
being
most
quiescent/mature
iAEC2s
proliferative/least
mature.
Cultures
either
did
not
generate
detectable
1
these
defined
conditions;
however,
subset
cocultured
fibroblasts
acquired
transitional
state
described
mice
humans
arise
during
fibrosis
or
following
injury.
Hence,
provide
direct
programs
engineered
models
that
can
harnessed
study
health
disease.
Advanced Materials,
Год журнала:
2023,
Номер
35(13)
Опубликована: Фев. 7, 2023
As
post-COVID
complications,
chronic
respiratory
diseases
are
one
of
the
foremost
causes
mortality.
The
quest
for
a
cure
this
recent
global
challenge
underlines
that
lack
predictive
in
vitro
lung
models
is
main
bottlenecks
pulmonary
preclinical
drug
development.
Despite
rigorous
efforts
to
develop
biomimetic
models,
current
cutting-edge
represent
compromise
numerous
technological
and
biological
aspects.
Most
advanced
still
"proof-of-concept"
phase
with
low
clinical
translation
findings.
On
other
hand,
advances
cellular
molecular
studies
mainly
based
on
relatively
simple
unrealistic
models.
Herein,
challenges
potential
strategies
toward
not
only
bioinspired
but
truly
discussed.
Immunological Reviews,
Год журнала:
2025,
Номер
330(1)
Опубликована: Март 1, 2025
ABSTRACT
Asthma
is
a
common
chronic
respiratory
disease
characterized
by
the
presence
of
airway
inflammation,
hyperresponsiveness,
and
mucus
hypersecretion.
Repeated
asthma
exacerbations
can
lead
to
progressive
remodeling
irreversible
airflow
obstruction.
Thus,
understanding
preventing
are
paramount
importance.
Although
multiple
endotypes
exist,
most
often
driven
type
2
inflammation.
New
therapies
that
target
specific
mediators
have
been
shown
reduce
frequency
but
incompletely
effective
in
significant
number
asthmatics.
Furthermore,
it
remains
unknown
whether
current
treatments
sustained
changes
or
if
targeting
additional
pathways
may
be
necessary
achieve
remission.
Activation
innate
immunity
initial
event
inflammatory
sequence
occurs
during
an
exacerbation.
However,
there
continue
critical
gaps
our
immune
response
exacerbating
factors.
In
this
review,
we
summarize
role
methods
used
study
them.
We
also
identify
potential
novel
therapeutic
targets
for
future
areas
investigation.
Physiology,
Год журнала:
2022,
Номер
37(5), С. 242 - 252
Опубликована: Июнь 6, 2022
The
intertwined
relationship
between
structure
and
function
has
been
key
to
understanding
human
organ
physiology
disease
pathogenesis.
An
organ-on-a-chip
(organ
chip)
is
a
bioengineered
microfluidic
cell
culture
device
lined
by
living
cells
tissues
that
recapitulates
organ-level
functions
in
vitro.
This
accomplished
recreating
organ-specific
tissue-tissue
interfaces
microenvironmental
biochemical
mechanical
cues
while
providing
dynamic
perfusion
through
endothelium-lined
vascular
channels.
In
this
review,
we
discuss
how
emerging
technology
contributed
the
of
lung
structure-function
relationships
at
cell,
tissue,
levels.