European Journal of Immunology,
Journal Year:
2024,
Volume and Issue:
54(6)
Published: April 9, 2024
Abstract
Chronic
thromboembolic
pulmonary
hypertension
(CTEPH)
is
a
debilitating
disease
characterized
by
thrombotic
occlusion
of
arteries
and
vasculopathy,
leading
to
increased
vascular
resistance
progressive
right‐sided
heart
failure.
Thrombotic
lesions
in
CTEPH
contain
CD68
+
macrophages,
increasing
evidence
supports
their
role
pathogenesis.
Macrophages
are
classically
divided
into
pro‐inflammatory
M1
macrophages
anti‐inflammatory
M2
which
involved
wound
healing
tissue
repair.
Currently,
the
phenotype
localization
within
largely
unknown.
In
our
study,
we
subclassified
patients
developing
fresh
thrombi
(FT)
organized
(OT),
based
on
degree
fibrosis
remodeling.
We
used
multiplex
immunofluorescence
histology
identify
immune
cell
infiltrates
CPTEH
patients.
Utilizing
software‐assisted
detection
quantification,
proportions
were
observed
OT
lesions,
compared
with
FT.
Strikingly,
CD206
INOS
−
significantly
higher
than
FT,
mainly
contained
unpolarized
macrophages.
Taken
together,
shift
from
FT
toward
an
expanded
population
OT,
indicating
dynamic
during
Cells,
Journal Year:
2023,
Volume and Issue:
12(17), P. 2193 - 2193
Published: Sept. 1, 2023
Idiopathic
pulmonary
fibrosis
(IPF)
is
a
lethal
interstitial
lung
disease
of
unknown
etiology
with
poor
prognosis.
It
chronic
and
progressive
that
has
distinct
radiological
pathological
pattern
from
common
pneumonia.
The
use
immunosuppressive
medication
was
shown
to
be
completely
ineffective
in
clinical
trials,
resulting
years
neglect
the
immune
component.
However,
recent
developments
fundamental
translational
science
demonstrate
cells
play
significant
regulatory
role
IPF,
macrophages
appear
among
most
crucial.
These
highly
plastic
generate
multiple
growth
factors
mediators
affect
initiation
progression
IPF.
In
this
review,
we
will
provide
an
update
on
IPF
through
systemic
discussion
various
mechanisms
involving
receptors,
cytokines,
metabolism,
epigenetics.
Frontiers in Physiology,
Journal Year:
2025,
Volume and Issue:
16
Published: Jan. 31, 2025
Precision-cut
lung
slices
(PCLS)
are
commonly
used
as
an
ex
vivo
model
to
study
fibrosis;
however,
traditional
models
lack
immune
cell
infiltration,
including
the
recruitment
of
monocytes
and
macrophages,
which
critical
for
inflammation
fibrosis.
To
address
this
limitation,
we
developed
novel
autologous
PCLS-immune
co-culture
that
better
replicate
processes
inflammation,
repair,
associated
with
Fibrotic
responses
nicotine,
cigarette
smoke
extract
(CSE),
a
fibrosis-inducing
cocktail
(FC)
were
first
evaluated
in
PCLS
containing
only
tissue-resident
upregulation
α-SMA-expressing
fibroblasts
confirmed
by
immunofluorescence
Western
blotting,
collagen
deposition
quantified
using
Sirius
Red
staining.
macrophage
recruitment,
employed
indirect
transwells
approximate
blood
vessel
function.
Chemotactic
studies
revealed
increased
migration
bone
marrow-derived
macrophages
(BMDMs)
toward
infiltration
into
CSE-injured
PCLS.
In
direct
simulating
repair
phase
fibrosis,
exposed
CSE
FC
showed
further
presence
BMDMs,
but
not
heterologous
ones.
These
findings
suggest
our
provide
platform
studying
involvement
fibrosis
offer
potential
developing
macrophage-targeted
therapeutic
strategies
pulmonary
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Feb. 3, 2025
Idiopathic
pulmonary
fibrosis
(IPF)
is
a
chronic
lung
disease
characterized
by
excessive
scarring
and
due
to
the
abnormal
accumulation
of
extracellular
matrix
components,
primarily
collagen.
This
study
aims
design
solve
an
optimal
control
problem
regulate
M2
macrophage
activity
in
IPF,
thereby
preventing
formation
controlling
anti-M1
agent.
The
research
models
diffusion
macrophages
inflamed
tissue
using
novel
dynamical
system
with
partial
differential
equation
(PDE)
constraints.
formulated
minimize
regulating
employs
two-step
process
discretization
followed
optimization,
utilizing
Galerkin
spectral
method
transform
PDE
into
algebraic
ordinary
equations
(ODEs).
then
solved
Pontryagin/s
minimum
principle,
canonical
Hamiltonian
equations,
extended
Riccati
equations.
numerical
simulations
indicate
that
without
control,
levels
increase
stabilize,
contributing
fibrosis.
In
contrast,
strategy
effectively
reduces
macrophages,
within
120
days.
results
highlight
potential
proposed
approach
modulating
repair
processes
mitigating
progression
IPF.
underscores
significance
targeting
employing
mathematical
methods
develop
innovative
therapies
for
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Feb. 25, 2025
Silicosis
and
asbestosis,
distinct
forms
of
pneumoconiosis,
manifest
progressive
interstitial
fibrosis
due
to
exposure
silica
dust
or
asbestos
fibers.
This
study
aimed
identify
potential
biomarkers
for
diagnosing
silicosis
while
also
evaluating
disease
severity
prognosis.
We
undertook
an
prospective
observational
involving
patients
with
asbestosis.
The
correlation
between
baseline
CC-chemokine
ligand
18
(CCL18),
CXC
motif
chemokine
13
(CXCL13),
osteopontin
(OPN),
periostin,
fibulin-3
clinical
variables
was
analyzed.
Diagnostic
sensitivity
evaluated
using
receiver
operating
characteristic
curves,
correlations
biomarker
levels
were
Multivariable
Cox
regression
assessed
the
concentrations'
strength
in
predicting
all-cause
mortality
Of
231
163
asbestosis
included
study,
29
(12.6%)
28
(17.2%)
died
within
five
years
follow-up
period.
Elevated
concentrations
CCL18,
CXCL13,
OPN
observed
compared
118
HCs.
accuracy
order,
OPN,
CXCL13.
Combining
CXCL13
enhanced
diagnostic
accuracy.
In
patients,
these
significantly
associated
lung
function
values.
However,
not
risk
factor
mortality.
stand
out
as
promising
Meanwhile,
may
be
used
evaluation
conditions.
Biomedicines,
Journal Year:
2025,
Volume and Issue:
13(4), P. 796 - 796
Published: March 26, 2025
Rationale:
The
role
of
the
innate
immune
system
in
idiopathic
pulmonary
fibrosis
(IPF)
remains
poorly
understood.
However,
a
functional
myeloid
compartment
is
required
to
remove
dying
cells
and
cellular
debris,
as
well
mediate
responses
against
pathogens.
Aberrant
macrophage
activity
has
been
described
patients
with
post-acute
sequelae
COVID
(PASC-F),
caveolin
scaffolding
domain
(CSD)
peptides
have
found
attenuate
inflammation
mouse
lung
injury
models.
Therefore,
we
examined,
for
first
time,
effects
CSD
peptide
LTI-2355
on
synthetic
properties
human
isolated
from
explant
tissue
donor
lungs
IPF
PASC-F
tissue.
Methods
Results:
CD45+
exhibited
an
impaired
capacity
clear
autologous
dead
debris.
uptake
pathogen-coated
bioparticles
was
both
fibrotic
patient
groups
independent
type
pathogen,
highlighting
intrinsic
cell
impairment.
improved
phagocytic
cells,
this
improvement
paired
decreased
proinflammatory
pro-fibrotic
activity.
also
shown
primarily
target
CD206-expressing
cells.
Conclusions:
Primary
exhibit
dysfunctional
that
are
modulated
by
LTI-2355.
treatment
resulted
significantly
reduced
sCD163,
IFN-α2,
IFN-γ,
IL-2,
IL-10,
IL-12p40,
MMP-1
supernatant.
This
study
highlights
additional
mechanism
action
progressive
disease.
Pharmacological Research,
Journal Year:
2025,
Volume and Issue:
216, P. 107756 - 107756
Published: April 29, 2025
Idiopathic
pulmonary
fibrosis
(IPF)
is
one
of
the
most
common
interstitial
lung
diseases
with
a
high
mortality
rate.
Calcaratarin
D
(CalD),
labdane
diterpenoid,
has
been
shown
to
possess
anti-inflammatory
properties.
The
present
study
evaluated
therapeutic
potential
CalD
in
fibrosis.
A
single
dose
bleomycin
(BLM,
2.5mg/kg)
was
instilled
intratracheally
mice
for
up
21
days
develop
Oral
(50mg/kg)
reduced
BLM-induced
inflammatory
cell
infiltration,
especially
pro-fibrotic
Arg1-expressing
macrophages
bronchoalveolar
lavage
fluid.
During
late
fibrotic
phase,
decreased
and
body
weight
loss.
In
addition,
ameliorated
histopathology,
collagen
deposition
mucus
hypersecretion,
improved
functions
BLM-exposed
mice.
Furthermore,
modulated
levels
pro-inflammatory
cytokines,
chemokines,
growth
factors
BAL
fluid
tissues.
mouse
lungs,
BLM
selectively
upregulated
Wnt10A
level
promoted
β-catenin
nuclear
translocation.
not
only
blocked
Wnt10A/β-catenin
signaling
pathway
but
also
markers
such
as
collagens,
α-SMA
FHL2.
normal
human
fibroblasts,
inhibited
TGF-β1-stimulated
Wnt/β-catenin
by
reducing
production,
upregulating
endogenous
Wnt
antagonist
DKK1
level,
dephosphorylating
ligand
co-receptor
LRP6,
preventing
YAP/TAZ
antifibrotic
action
be
dependent
on
its
α,β-unsaturated
γ-butyrolactone
structure
that
essential
form
covalent
interaction
cellular
protein
targets.
Our
results
imply
could
novel
agent
IPF,
acting
through
blockade
pathway.