Transcriptomic profiles of monocyte-derived macrophages exposed to SARS-CoV-2 VOCs reveal immune-evasion escape driven by delta
Journal of Translational Medicine,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Feb. 4, 2025
Since
the
breakout
of
COVID-19,
mutated
forms
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
have
shown
enhanced
rates
transmission
and
adaptation
to
humans.
The
variants
concern
(VOC),
designated
Alpha,
Beta,
Gamma,
Delta,
Omicron
emerged
independent
one
another,
in
turn
rapidly
became
dominant.
success
each
VOC,
as
well
virus
fitness,
were
enabled
by
altered
intrinsic
functional
properties
and,
reasonably,
antigenicity
changes,
conferring
ability
evade
a
primed
immune
response.
We
analysed
gene
expression
profiles
monocyte-derived
macrophages
(MDM)
isolated
from
whole
blood
healthy
participants
exposed
5
different
SARS-CoV-2
VOC:
D614G,
Alpha
(B.1.1.7),
Gamma
(P1),
Delta
(B.1.617.2),
BA.1
(B.1.1.529),
HCoV-OC43
strain,
already
present
population
before
pandemic.
Whole
transcriptome
RNA-Seq,
for
both
coding
non-coding
RNAs,
was
then
made.
After
exposure
VOC
MDM,
we
initially
assessed
presence
viral
transcripts
confirm
entry.
RNA-Seq
data
observed
significant
deregulation
RNAs.
In
particular,
our
analysis
showed
up-regulation
several
genes
involved
immunological
processes,
such
PARP9/PARP14
axes,
variants.
Surprisingly,
that
variant
exhibited
transcriptional
profile
more
similar
naïve
control
group,
while
intermediate
differentially
expressed
(DEGs)
between
two
groups.
By
checking
canonical
markers
M1/M2
differentiation
states,
did
not
observe
any
variant,
suggesting
an
M0
status,
comparable
group.
Finally,
3
main
types
RNAs
(ncRNAs):
long
(lncRNAs),
microRNAs
(miRNAs),
small
nucleolar
(snoRNAs),
some
which
are
common
coronaviruses,
specific
SARS-CoV-2.
SARS-CoV-2-dependent
alteration
macrophage
(MDM)-infected
cells
can
be
linked
chronological
order
variants'
appearance
human
population.
Our
suggest
evolution
modulating
host
response,
with
strong
change
pace
beginning
advent
variant.
MDMs
failure
activation
adaptive
this
correlates
symptoms
developed
people
affected
Language: Английский
Cationic liposomes encapsulating IL-2 selectively induce apoptosis and significantly reduce the secretion of cytokines on M1-murine polarized macrophages
Cytokine,
Journal Year:
2025,
Volume and Issue:
189, P. 156903 - 156903
Published: Feb. 28, 2025
Language: Английский
SARS-CoV-2 nucleocapsid protein induces a Mincle-dependent macrophage inflammatory response in acute kidney injury
Ruizhi Tan,
No information about this author
Wenjing Zhao,
No information about this author
Jing Gao
No information about this author
et al.
Inflammation Research,
Journal Year:
2025,
Volume and Issue:
74(1)
Published: April 17, 2025
Language: Английский
Angiotensin-(1–7) decreases inflammation and lung damage caused by betacoronavirus infection in mice
Inflammation Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Sept. 18, 2024
Language: Английский
The role of epithelial-mesenchymal transition in pulmonary fibrosis: lessons from idiopathic pulmonary fibrosis and COVID-19
Reyhaneh Niayesh‐Mehr,
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Mojtaba Kalantar,
No information about this author
Giulio Bontempi
No information about this author
et al.
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Nov. 13, 2024
Despite
the
tremendous
advancements
in
knowledge
of
pathophysiology
and
clinical
aspects
SARS-CoV-2
infection,
still
many
issues
remain
unanswered,
especially
long-term
effects.
Mounting
evidence
suggests
that
pulmonary
fibrosis
(PF)
is
one
most
severe
complications
associated
with
COVID-19.
Therefore,
understanding
molecular
mechanisms
behind
its
development
helpful
to
develop
successful
therapeutic
strategies.
Epithelial
mesenchymal
transition
(EMT)
cell
specific
variants
endothelial
(EndMT)
mesothelial
(MMT)
are
physio-pathologic
cellular
reprogramming
processes
induced
by
several
infectious,
inflammatory
biomechanical
stimuli.
Cells
undergoing
EMT
acquire
invasive,
profibrogenic
proinflammatory
activities
secreting
extracellular
mediators.
Their
activity
has
been
implicated
pathogenesis
PF
a
variety
lung
disorders,
including
idiopathic
(IPF)
Aim
this
article
provide
an
updated
survey
mechanisms,
emphasis
on
EMT-related
processes,
genesis
IFP
Language: Английский
Hypotensive drugs mitigate the high-sodium diet-induced pro-inflammatory activation of mouse macrophages in vivo
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
175, P. 116648 - 116648
Published: April 26, 2024
Nowadays,
there
is
an
increasing
emphasis
on
the
need
to
alleviate
chronic
inflammatory
response
effectively
treat
hypertension.
However,
are
still
gaps
in
our
understanding
how
achieve
this.
Therefore,
research
interaction
of
antihypertensive
drugs
with
immune
system
extremely
interesting,
since
their
therapeutic
effect
could
partly
result
from
amelioration
hypertension-related
inflammation,
which
macrophages
seem
play
a
pivotal
role.
Thus,
current
comprehensive
studies
have
investigated
impact
repeatedly
administered
hypotensive
(captopril,
olmesartan,
propranolol,
carvedilol,
amlodipine,
verapamil)
macrophage
functions
innate
and
adaptive
immunity,
as
well
if
drug-induced
effects
affected
by
high-sodium
diet
(HSD),
one
key
environmental
risk
factors
Although
assayed
medications
increased
generation
reactive
oxygen
nitrogen
intermediates
standard
fed
donors,
they
reversed
HSD-induced
enhancing
oxidative
burst
secretion
pro-inflammatory
cytokines.
On
other
hand,
some
phagocytic
activity
expression
surface
markers
involved
antigen
presentation,
translated
into
enhanced
ability
activate
B
cells
for
antibody
production.
Moreover,
augmented
function
effector
phase
contact
hypersensitivity
reaction,
but
suppressed
sensitization
cell-mediated
under
HSD
conditions.
Our
findings
contribute
recognition
mechanisms,
excessive
sodium
intake
affects
hypertensive
individuals,
provide
evidence
that
mitigate
most
adverse
effects,
suggesting
additional
protective
activity.
Language: Английский
SARS-CoV-2 Modulation of HIV Latency Reversal in a Myeloid Cell Line: Direct and Bystander Effects
Patricio Jarmoluk,
No information about this author
Franco Agustín Sviercz,
No information about this author
Cintia Cevallos
No information about this author
et al.
Viruses,
Journal Year:
2024,
Volume and Issue:
16(8), P. 1310 - 1310
Published: Aug. 17, 2024
Coronavirus
disease
2019
(COVID-19)
might
impact
progression
in
people
living
with
HIV
(PLWH),
including
those
on
effective
combination
antiretroviral
therapy
(cART).
These
individuals
often
experience
chronic
conditions
characterized
by
proviral
latency
or
low-level
viral
replication
CD4+
memory
T
cells
and
tissue
macrophages.
Pro-inflammatory
cytokines,
such
as
TNF-α,
IL-1β,
IL-6,
IFN-γ,
can
reactivate
provirus
expression
both
primary
cell
lines.
cytokines
are
elevated
infected
SARS-CoV-2,
the
virus
causing
COVID-19.
However,
it
is
still
unknown
whether
SARS-CoV-2
modulate
reactivation
cells.
Here,
we
report
that
exposure
of
chronically
HIV-1-infected
myeloid
line
U1
to
two
different
isolates
(ancestral
BA.5)
reversed
its
latent
state
after
24
h.
We
also
observed
human
monocyte-derived
macrophages
(MDM)
initially
drove
their
polarization
towards
an
M1
phenotype,
which
shifted
M2
over
time.
This
effect
was
associated
soluble
factors
released
during
initial
phase
reactivated
production
cells,
like
MDM
stimulated
TLR
agonist
resiquimod.
Our
study
suggests
SARS-CoV-2-induced
systemic
inflammation
interaction
could
influence
HIV-1
PLWH.
Language: Английский
Angiotensin-(1-7) decreases inflammation and lung damage caused by betacoronavirus infection in mice
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: June 18, 2024
Abstract
Objective:
Pro-resolving
molecules,
including
the
peptide
Angiotensin-(1-7)
[Ang-(1-7)],
have
potential
adjunctive
therapy
for
infections.
Here
we
evaluate
actions
of
Ang-(1-7)
in
betacoronavirus
infection
mice.
Methods:
C57BL/6
mice
were
infected
intranasally
with
murine
MHV-3
and
K18-hACE2
SARS-CoV-2.
Mice
treated
(30
μg/mouse,
i.p.)
at
24-,
36-,
48-hours
post-infection
(hpi)
or
24,
36,
48,
72,
96
h.
For
lethality
evaluation,
one
additional
dose
was
given
120
hpi.
At
3-
5-days
post-
(dpi)
blood
cell,
inflammatory
mediators,
viral
loads,
lung
histopathology
evaluated.
Results:
Ang-(1-7)
rescued
lymphopenia
MHV-infected
mice,
decreased
airways
leukocyte
infiltration
damage
5-dpi.
The
levels
pro-inflammatory
cytokines
virus
titers
plasma
by
during
MHV
infection.
improved
function
increased
survival
rates
Notably,
treatment
SARS-CoV-2
restored
lymphocytes
to
baseline,
weight
loss,
titters
cytokines,
resulting
improvement
pulmonary
clinical
scores.
Conclusion:
protected
from
death
infections
modulating
inflammation,
hematological
parameters
enhancing
clearance.
Language: Английский
Role of T Helper 1 in COVID-19 Pathogenesis: Foe or Friend
International Journal of Enteric Pathogens,
Journal Year:
2023,
Volume and Issue:
11(4), P. 140 - 150
Published: Nov. 30, 2023
Cytokines
produced
by
T
helper
cells
(Th
cells)
have
essential
roles
in
the
body’s
defense
against
viruses.
Inadequate
and
high
levels
of
specific
cytokines
can
side
effects.
This
literature
review
article
discusses
mechanisms
Th1
responses
SARS-CoV-2
sheds
light
on
pivotal
role
various
inflammatory
markers
COVID-19-related
complications.
The
latest
literary
works
relevant
to
this
study
were
carefully
chosen
evaluated.
Extensive
searches
conducted
across
multiple
databases,
such
as
Scopus,
PubMed,
Google
Scholar,
ScienceDirect.
After
evaluating
existing
literature,
it
has
been
observed
that
unregulated
immune
result
heightened
inflammation.
Recent
studies
provided
proof
occurrence
cytokine
storms
significantly
contribute
severity
COVID-19,
ultimately
resulting
multi-organ
failure
loss
life.
Factors
influence
cell
response
its
impact
COVID-19
include
timing
response,
pre-existing
conditions,
viral
load,
genetic
susceptibility.
Ultimately,
effectively
managing
storm,
we
potential
greatly
reduce
number
deaths
caused
virus.
Language: Английский