Journal of Intensive Care Medicine,
Год журнала:
2023,
Номер
38(11), С. 1003 - 1014
Опубликована: Май 24, 2023
Although
corticosteroids
have
become
the
standard
of
care
for
patients
with
coronavirus
disease-2019
(COVID-19)
on
supplemental
oxygen,
there
is
growing
evidence
differential
treatment
response.
This
study
aimed
to
evaluate
if
was
an
association
between
biomarker-concordant
corticosteroid
and
COVID-19
outcomes.This
registry-based
cohort
included
adult
hospitalized
January
2020
December
2021
from
109
institutions.
Patients
available
C-reactive
protein
(CRP)
levels
within
48
h
admission
were
evaluated.
Those
steroids
before
admission,
stayed
in
hospital
<48
h,
or
not
oxygen
support
excluded.
Corticosteroid
given
high
baseline
CRP
≥150
mg/L
withheld
low
(<150
mg/L)
vice-versa
considered
discordant
(low
steroids,
without
steroids).
Hospital
mortality
primary
outcome.
Sensitivity
analyses
conducted
using
varying
level
thresholds.
The
model
interaction
tested
determine
steroid
effectiveness
increasing
levels.Corticosteroid
1778
(49%)
1835
(51%).
concordant
group
consisted
higher-risk
than
group.
After
adjusting
covariates,
odds
in-hospital
significantly
lower
(odds
ratio
[95%
confidence
interval
(C.I.)]
=
0.71
[0.51,
0.98]).
Similarly,
adjusted
difference
significant
at
thresholds
100
200
C.I.]
0.70
[0.52,
0.95]
0.57
[0.38,
0.85],
respectively),
use
associated
need
invasive
ventilation
threshold
0.52
[0.30,
0.91]).
In
contrast,
no
outcome
benefit
observed
50.
When
tested,
more
effective
reducing
as
increased.Biomarker-concordant
severe
COVID-19.
Viruses,
Год журнала:
2021,
Номер
13(7), С. 1192 - 1192
Опубликована: Июнь 22, 2021
Despite
the
slow
evolutionary
rate
of
SARS-CoV-2
relative
to
other
RNA
viruses,
its
massive
and
rapid
transmission
during
COVID-19
pandemic
has
enabled
it
acquire
significant
genetic
diversity
since
first
entered
human
population.
This
led
emergence
numerous
variants,
some
them
recently
being
labeled
“variants
concern”
(VOC),
due
their
potential
impact
on
transmission,
morbidity/mortality,
evasion
neutralization
by
antibodies
elicited
infection,
vaccination,
or
therapeutic
application.
The
evade
is
result
target
epitopes
generated
accumulation
mutations
in
spike
protein.
While
three
globally
recognized
VOCs
(Alpha
B.1.1.7,
Beta
B.1.351,
Gamma
P.1)
remain
sensitive
albeit
at
reduced
levels
sera
convalescent
individuals
recipients
several
anti-COVID19
vaccines,
effect
variability
much
more
evident
capacity
monoclonal
antibodies.
newly
VOC
Delta
lineage
B.1.617.2,
as
well
locally
accepted
(Epsilon
B.1.427/29-US
B1.1.7
with
E484K-UK)
are
indicating
necessity
close
monitoring
new
variants
a
global
level.
characteristics,
mutational
patterns,
role
play
immune
summarized
this
review.
Biomedicine & Pharmacotherapy,
Год журнала:
2021,
Номер
145, С. 112419 - 112419
Опубликована: Ноя. 12, 2021
Interleukin-6
(IL-6)
is
a
multi-tasking
cytokine
that
represents
high
activity
in
patients
with
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
and
cancer.
High
concentration
of
this
pleiotropic
accounts
for
hyperinflammation
storm,
related
to
multi-organ
failure
SARS-CoV-2
induced
disease.
IL-6
promotes
lymphopenia
increases
C-reactive
protein
(CRP)
such
cases.
However,
blockade
not
full-proof
complete
response.
Hypoxia,
hypoxemia,
aberrant
angiogenesis
chronic
inflammation
are
inter-related
events
occurring
as
response
the
stimulatory
effect
on
activity.
Taking
both
pro-
anti-inflammatory
activities
will
make
complex
targeting
patient
The
aim
review
was
discuss
about
interactions
within
body
disease
who
representing
levels,
determine
whether
inhibition
therapy
effective
or
not.
We
also
address
targeted
therapies
cancer
have
Journal of Inflammation Research,
Год журнала:
2023,
Номер
Volume 16, С. 2209 - 2222
Опубликована: Май 1, 2023
Aim:The
aim
of
our
retrospective
study
was
search
for
new
prognostic
parameters,
which
can
help
quickly
and
cheaply
identify
patients
with
risk
severe
course
SARS-CoV-2
infection.
Materials
Methods:The
following
peripheral
blood
combination
biomarkers
were
calculated:
NLR
(neutrophil/lymphocytes
ratio),
LMR
(lymphocyte/monocyte
PLR
(platelet/lymphocyte
dNLR
(neutrophils/(white
cells
-neutrophils)),
NLPR
(neutrophil/(lymphocyte
×
platelet
ratio))
in
374
who
admitted
to
the
Temporary
Hospital
no
2
Clinical
Bialystok
(Poland)
COVID-19.The
divided
into
four
groups
depending
on
severity
COVID-19
using
MEWS
classification.
Results:The
significantly
increased
COVID-19,
according
score.The
AUC
assessed
parameters
higher
predicting
death
COVID-19:
(0.656,
p=0.0018,
cut-off=6.22),dNLR
(0.615,
p=0.02,
cut-off=3.52)and
(0.609,
p=0.03,
cut-off=2.06).Multivariate
COX
regression
analysis
showed
that
median
above
5.56
(OR:
1.050,
P=0.002),
below
2.23
1.021,
P=0.011),
age
>75
years
old
1.072,
P=0.000)
had
a
significant
association
high
during
COVID-19.
Conclusion:Our
results
indicate
NLR,
dNLR,
calculated
admission
hospital
easy
more
COVID-19.Increase
decrease
have
predictive
value
patient's
mortality
might
be
potential
biomarker
patients.
Cell Death and Differentiation,
Год журнала:
2024,
Номер
31(5), С. 544 - 557
Опубликована: Март 21, 2024
Abstract
The
dysregulated
immune
response
and
inflammation
resulting
in
severe
COVID-19
are
still
incompletely
understood.
Having
recently
determined
that
aberrant
death-ligand-induced
cell
death
can
cause
lethal
inflammation,
we
hypothesized
this
process
might
also
or
contribute
to
inflammatory
disease
lung
failure
following
SARS-CoV-2
infection.
To
test
hypothesis,
developed
a
novel
mouse-adapted
model
(MA20)
recapitulates
key
pathological
features
of
COVID-19.
Concomitantly
with
occurrence
FasL
expression
was
significantly
increased
on
monocytic
macrophages
NK
cells
the
lungs
MA20-infected
mice.
Importantly,
therapeutic
inhibition
markedly
survival
both,
young
old
mice
coincident
substantially
reduced
their
lungs.
Intriguingly,
bronchoalveolar
lavage
fluid
critically-ill
patients.
Together,
these
results
identify
as
crucial
host
factor
driving
immuno-pathology
underlies
severity
lethality,
imply
patients
may
benefit
from
FasL.
Emerging Microbes & Infections,
Год журнала:
2022,
Номер
11(1), С. 2393 - 2404
Опубликована: Сен. 7, 2022
The
coronavirus
disease
2019
(COVID-19)
pandemic,
caused
by
severe
acute
respiratory
syndrome
2
(SARS-CoV-2),
poses
an
imminent
threat
to
humanity.
SARS-CoV-2
invades
host
cells,
causing
a
failure
of
immune
recognition.
Instead
effective
antiviral
immunological
response
after
invasion,
the
cascading
pathological
COVID-19,
especially
in
disease,
is
exacerbated
overt
inflammatory
and
suppression
SARS-CoV-2–specific
responses.
As
known,
excessive
inflammation
leads
pathophysiological
changes
virus-infected
tissues
or
organs,
manifested
imbalanced
responses,
cytokine
storm,
aggressive
neutrophil
activation,
ultimately
leading
lung
damage,
such
as
alveolar
endotheliitis,
fluid
overload.
However,
triggers
consequences
disruption
system
homeostasis
underlying
mechanisms
uncontrolled
immunopathology
following
viral
infection
remain
unclear.
Here,
we
review
dynamic
systemic
progression
from
imbalance
cell-mediated
responses
COVID-19
injury.
Our
understanding
key
involved
pathogenesis
critical
for
development
therapeutic
agents
optimize
strategies.
Frontiers in Immunology,
Год журнала:
2022,
Номер
13
Опубликована: Апрель 27, 2022
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
is
the
causative
agent
of
ongoing
disease
2019
(COVID-19)
pandemic.
Viral
replication
in
tract
induces
death
infected
cells
and
release
pathogen-
associated
molecular
patterns
(PAMPs).
PAMPs
give
rise
to
local
inflammation,
increasing
secretion
pro-
inflammatory
cytokines
chemokines,
which
attract
immune
from
blood
into
lung.
In
most
individuals,
lung-recruited
clear
infection,
response
retreats.
However,
some
cases,
a
dysfunctional
occurs,
triggers
cytokine
storm
lung,
leading
distress
(ARDS).
COVID-19
characterized
by
an
impaired
innate
adaptive
massive
expansion
myeloid-derived
suppressor
(MDSCs).
MDSCs
function
as
protective
regulators
response,
protecting
host
over-immunoreactivity
hyper-inflammation.
under
certain
conditions,
such
chronic
inflammation
cancer,
could
exert
detrimental
role.
Accordingly,
early
able
predict
fatal
outcome
infection.
Here,
we
review
recent
data
on
during
COVID-19,
discussing
how
they
can
influence
course
whether
be
considered
biomarker
possible
targets
for
new
therapeutic
approaches.