Journal of Clinical Investigation,
Journal Year:
2025,
Volume and Issue:
135(1)
Published: Jan. 1, 2025
Single-cell
transcriptomics
applied
to
cerebrospinal
fluid
(CSF)
for
elucidating
the
pathophysiology
of
neurologic
diseases
has
produced
only
a
preliminary
characterization
CSF
immune
cells.
derives
from
and
borders
central
nervous
system
(CNS)
tissue,
allowing
comprehensive
accounting
cell
types
along
with
their
relative
abundance
immunologic
profiles
relevant
CNS
diseases.
Using
integration
techniques
publicly
available
datasets
in
combination
our
own
studies,
we
generated
compendium
139
subjects
encompassing
135
58
blood
samples.
Healthy
individuals
across
wide
range
diseases,
such
as
multiple
sclerosis
(MS),
Alzheimer's
disease,
Parkinson's
COVID-19,
autoimmune
encephalitis,
were
included.
We
found
differences
lymphocyte
myeloid
subset
frequencies
different
well
distribution
between
CSF.
identified
what
believe
be
new
AREG+
dendritic
cells
exclusive
that
was
more
abundant
MS
compared
healthy
controls.
Finally,
transcriptional
states
microglia-like
lymphoid
subsets
elucidated.
Altogether,
have
created
reference
single-cell
profiling
useful
scientific
community
future
studies
on
Frontiers in Pharmacology,
Journal Year:
2022,
Volume and Issue:
12
Published: Jan. 12, 2022
Severe
Acute
Respiratory
Syndrome
Coronavirus—2
(SARS
CoV-2)
has
resulted
in
the
global
spread
of
Coronavirus
Disease
2019
(COVID-19)
and
an
increase
complications
including
Distress
(ARDS).
Due
to
lack
therapeutic
options
for
Syndrome,
recent
attention
focused
on
differentiating
hyper-
hypo-inflammatory
phenotypes
ARDS
help
define
effective
strategies.
Interleukin
8
(IL-8)
is
a
pro-inflammatory
cytokine
that
role
neutrophil
activation
been
identified
within
pathogenesis
progression
this
disease.
The
aim
review
highlight
IL-8
as
biomarker
prognostic
factor
modulating
hyperinflammatory
response
ARDS.
crucial
lung
inflammation
disease
might
suggest
possible
new
target
efficiently
modulate
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: April 7, 2022
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
has
resulted
in
countless
infections
and
caused
millions
of
deaths
since
its
emergence
2019.
Coronavirus
disease
2019
(COVID-19)-associated
mortality
is
by
uncontrolled
inflammation,
aberrant
immune
response,
cytokine
storm,
an
imbalanced
hyperactive
system.
The
storm
further
results
multiple
organ
failure
lung
immunopathology.
Therefore,
any
potential
treatments
should
focus
on
the
direct
elimination
viral
particles,
prevention
strategies,
mitigation
(hyperactive)
This
review
focuses
secretions
innate
adaptive
responses
against
COVID-19,
including
interleukins,
interferons,
tumor
necrosis
factor-alpha,
other
chemokines.
In
addition
to
focus,
we
discuss
immunotherapeutic
approaches
based
relevant
pathophysiological
features,
systemic
response
SARS-CoV-2,
data
from
recent
clinical
trials
experiments
COVID-19-associated
storm.
Prompt
use
these
cytokines
as
diagnostic
markers
aggressive
management
can
help
determine
morbidity
mortality.
prophylaxis
rapid
appear
significantly
improve
outcomes.
For
reasons,
this
study
aims
provide
advanced
information
facilitate
innovative
strategies
survive
COVID-19
pandemic.
Abstract
The
novel
coronavirus
disease
2019
(COVID-19)
pandemic
has
spread
worldwide,
and
finding
a
safe
therapeutic
strategy
effective
vaccine
is
critical
to
overcoming
severe
acute
respiratory
syndrome
2
(SARS-CoV-2).
Therefore,
elucidation
of
pathogenesis
mechanisms,
especially
entry
routes
SARS-CoV-2
may
help
propose
antiviral
drugs
vaccines.
Several
receptors
have
been
demonstrated
for
the
interaction
spike
(S)
protein
with
host
cells,
including
angiotensin-converting
enzyme
(ACE2),
ephrin
ligands
Eph
receptors,
neuropilin
1
(NRP-1),
P2X7,
CD147.
expression
these
in
central
nervous
system
(CNS)
make
CNS
prone
invasion,
leading
neurodegenerative
diseases.
present
review
provides
potential
pathological
mechanisms
infection
CNS,
cytokines
involved
neuroinflammatory
conditions.
Moreover,
it
explains
several
disorders
associated
COVID-19.
Finally,
we
suggest
inflammasome
JaK
inhibitors
as
strategies
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
12
Published: Jan. 14, 2022
The
poor
outcome
of
the
coronavirus
disease-2019
(COVID-19),
caused
by
SARS-CoV-2,
is
associated
with
systemic
hyperinflammatory
response
and
immunopathology.
Although
inflammasome
oxidative
stress
have
independently
been
implicated
in
COVID-19,
it
poorly
understood
whether
these
two
pathways
cooperatively
contribute
to
disease
severity.
Herein,
we
found
an
enrichment
CD14highCD16-
monocytes
displaying
activation
evidenced
caspase-1/ASC-speck
formation
severe
COVID-19
patients
when
compared
mild
ones
healthy
controls,
respectively.
Those
cells
also
showed
aberrant
levels
mitochondrial
superoxide
lipid
peroxidation,
both
hallmarks
response,
which
strongly
correlated
caspase-1
activity.
In
addition,
that
NLRP3
inflammasome-derived
IL-1β
secretion
SARS-CoV-2-exposed
vitro
was
partially
dependent
on
peroxidation.
Importantly,
altered
responses
persisted
after
short-term
patient
recovery.
Collectively,
our
findings
suggest
stress/NLRP3
signaling
pathway
as
a
potential
target
for
host-directed
therapy
mitigate
early
hyperinflammation
its
long-term
outcomes.
Journal of Virology,
Journal Year:
2022,
Volume and Issue:
96(6)
Published: Feb. 2, 2022
Given
the
current
coronavirus
disease
2019
(COVID-19)
pandemic,
coinfection
of
severe
acute
respiratory
syndrome
2
(SARS-CoV-2)
and
influenza
A
virus
(IAV)
is
a
major
concern
for
public
health.
However,
immunopathogenic
events
occurring
with
coinfections
SARS-CoV-2
IAV
remain
unclear.
Here,
we
report
pathogenic
immunological
consequences
H1N1
in
K18-hACE2
transgenic
mouse
model.
Compared
single
infection
or
IAV,
not
only
prolonged
primary
period
but
also
increased
immune
cell
infiltration
inflammatory
cytokine
levels
bronchoalveolar
lavage
fluid
leading
to
pneumonia
lung
damage.
Moreover,
caused
lymphopenia
peripheral
blood,
resulting
reduced
total
IgG,
neutralizing
antibody
titers,
CD4
Nature Immunology,
Journal Year:
2023,
Volume and Issue:
24(4), P. 604 - 611
Published: March 6, 2023
Abstract
Infection
with
severe
acute
respiratory
syndrome
coronavirus
2
associates
diverse
symptoms,
which
can
persist
for
months.
While
antiviral
antibodies
are
protective,
those
targeting
interferons
and
other
immune
factors
associated
adverse
disease
2019
(COVID-19)
outcomes.
Here
we
discovered
that
against
specific
chemokines
were
omnipresent
post-COVID-19,
favorable
outcome
negatively
correlated
the
development
of
long
COVID
at
1
yr
post-infection.
Chemokine
also
present
in
HIV-1
infection
autoimmune
disorders,
but
they
targeted
different
compared
COVID-19.
Monoclonal
derived
from
COVID-19
convalescents
bound
to
chemokine
N-loop
impaired
cell
migration.
Given
role
orchestrating
trafficking,
naturally
arising
may
modulate
inflammatory
response
thus
bear
therapeutic
potential.
Journal of Medical Virology,
Journal Year:
2023,
Volume and Issue:
95(4)
Published: April 1, 2023
Abstract
In
patients
with
severe
COVID‐19,
acute
respiratory
distress
syndrome
(ARDS),
multiple
organ
dysfunction
(MODS),
and
even
mortality
can
result
from
cytokine
storm,
which
is
a
hyperinflammatory
medical
condition
caused
by
the
excessive
uncontrolled
release
of
pro‐inflammatory
cytokines.
High
levels
numerous
crucial
cytokines,
such
as
interleukin‐1
(IL‐1),
IL‐2,
IL‐6,
tumor
necrosis
factor‐α,
interferon
(IFN)‐γ,
IFN‐induced
protein
10
kDa,
granulocyte‐macrophage
colony‐stimulating
factor,
monocyte
chemoattractant
protein‐1,
IL‐10
so
on,
have
been
found
in
COVID‐19.
They
participate
cascade
amplification
pathways
responses
through
complex
inflammatory
networks.
Here,
we
review
involvements
these
critical
cytokines
SARS‐CoV‐2
infection
discuss
their
potential
roles
triggering
or
regulating
help
to
understand
pathogenesis
So
far,
there
rarely
effective
therapeutic
strategy
for
storm
besides
using
glucocorticoids,
proved
fatal
side
effects.
Clarifying
key
involved
network
will
develop
an
ideal
intervention,
neutralizing
antibody
certain
inhibitor
some
signal
pathways.
Heliyon,
Journal Year:
2024,
Volume and Issue:
10(8), P. e29686 - e29686
Published: April 1, 2024
Monocytes
and
macrophages
are
essential
components
of
innate
immune
system
have
versatile
roles
in
homeostasis
immunity.
These
phenotypically
distinguishable
mononuclear
phagocytes
play
distinct
different
stages,
contributing
to
the
pathophysiology
various
forms
making
them
a
potentially
attractive
therapeutic
target
inflammatory
conditions.
Several
pieces
evidence
supported
role
cell
surface
receptors
expressed
on
these
cells
their
downstream
signaling
molecules
initiating
perpetuating
response.
In
this
review,
we
discuss
current
understanding
monocyte
macrophage
biology
inflammation,
highlighting
chemoattractants,
inflammasomes,
integrins
function
monocytes
during
events
inflammation.
This
review
also
covers
recent
interventions
targeting
at
cellular
molecular
levels.