Critical Care Medicine,
Год журнала:
2019,
Номер
48(2), С. e98 - e106
Опубликована: Ноя. 17, 2019
Corticosteroids
may
be
beneficial
in
sepsis,
but
uncertainty
remains
over
their
effects
severe
influenza.
This
systematic
review
updates
the
current
evidence
regarding
corticosteroids
treatment
of
influenza
and
examines
effect
dose
on
outcome.
Annals of the New York Academy of Sciences,
Год журнала:
2018,
Номер
1437(1), С. 57 - 67
Опубликована: Май 11, 2018
Abstract
Neuropsychiatric
disorders
(i.e.,
mood
and
schizophrenia)
inflammation
are
closely
intertwined,
possibly
powering
each
other
in
a
bidirectional
loop.
Depression
facilitates
inflammatory
reactions
promotes
depression
neuropsychiatric
disorders.
Patients
with
exhibit
all
cardinal
features
of
inflammation,
including
increased
circulating
levels
inducers,
activated
sensors,
mediators
targeting
tissues.
Inflammation
may
contribute
to
the
pathophysiology
clinical
progression
these
Of
note,
proinflammatory
cytokines
modulate
behavior
cognition
by
reducing
brain
monoamine
levels,
activating
neuroendocrine
responses,
promoting
excitotoxicity
(increased
glutamate
levels),
impairing
plasticity.
What
sources
this
chronic
inflammation?
Increasing
evidence
indicates
that
changes
regulation,
metabolism,
diet/microbiota,
negative
health
behaviors
important
triggers
inflammation.
Finally,
recent
data
indicate
early‐life
stress
is
associated
overt
prior
development
Cell Research,
Год журнала:
2021,
Номер
31(3), С. 272 - 290
Опубликована: Янв. 21, 2021
Abstract
How
the
innate
and
adaptive
host
immune
system
miscommunicate
to
worsen
COVID-19
immunopathology
has
not
been
fully
elucidated.
Here,
we
perform
single-cell
deep-immune
profiling
of
bronchoalveolar
lavage
(BAL)
samples
from
5
patients
with
mild
26
critical
in
comparison
BALs
non-COVID-19
pneumonia
normal
lung.
We
use
pseudotime
inference
build
T-cell
monocyte-to-macrophage
trajectories
model
gene
expression
changes
along
them.
In
COVID-19,
CD8
+
resident-memory
(T
RM
)
CD4
T-helper-17
H17
cells
undergo
active
(presumably
antigen-driven)
expansion
towards
end
trajectory,
are
characterized
by
good
effector
functions,
while
they
remain
more
naïve.
Vice
versa,
T-cells
T-helper-1
characteristics
H1
-like)
expressing
exhaustion
markers
EX
enriched
halfway
their
where
also
exhibit
show
evidence
inflammation-associated
stress
at
trajectories.
Monocyte-to-macrophage
that
chronic
hyperinflammatory
monocytes
alveolar
macrophages,
otherwise
anti-inflammatory
antigen-presenting
characteristics,
depleted.
contribute
an
ATP-purinergic
signaling-inflammasome
footprint
could
enable
associated
fibrosis
disease-severity.
Finally,
viral
RNA-tracking
reveals
infected
lung
epithelial
cells,
a
significant
proportion
neutrophils
macrophages
involved
clearance.
Frontiers in Psychiatry,
Год журнала:
2019,
Номер
10
Опубликована: Март 11, 2019
Early
life
stressors
display
a
high
universal
prevalence
and
constitute
major
public
health
problem.
Prolonged
psychoneurobiological
alterations
as
sequelae
of
early
stress
(ELS)
could
represent
developmental
risk
factor
mediate
for
disease,
leading
to
higher
physical
mental
morbidity
rates
in
later
life.
ELS
exert
programming
effect
on
sensitive
neuronal
brain
networks
related
the
response
during
critical
periods
development
thus
lead
enduring
hyper-
or
hypo-activation
system
altered
glucocorticoid
signaling.
In
addition,
emotional
autonomic
reactivity,
circadian
rhythm
disruption,
functional
structural
changes
brain,
well
immune
metabolic
dysregulation
have
been
lately
identified
important
factors
chronically
impaired
homeostatic
balance
after
ELS.
Furthermore,
human
genetic
background
epigenetic
modifications
through
stress-related
gene
expression
interact
with
these
explain
inter-individual
variation
vulnerability
resilience
stress.
This
narrative
review
presents
relevant
evidence
from
mainly
research
ten
most
acknowledged
neurobiological
allostatic
pathways
exerting
adverse
effects
even
decades
(hypothalamic-pituitary-adrenal
axis,
nervous
system,
inflammation,
oxidative
stress,
cardiovascular
gut
microbiome,
sleep
genetics,
epigenetics,
structural,
correlates).
Although
findings
back
causal
relation
between
psychobiological
maladjustment
life,
precise
trajectories
their
temporal
coincidence
has
not
elucidated
yet.
Future
studies
should
prospectively
investigate
putative
mediators
sequence,
while
considering
potentially
delayed
time-frame
phenotypical
expression.
Better
screening
strategies
are
needed
better
individual
prevention
treatment.
Nature Communications,
Год журнала:
2020,
Номер
11(1)
Опубликована: Июль 17, 2020
Abstract
Tumors
subvert
immune
cell
function
to
evade
responses,
yet
the
complex
mechanisms
driving
evasion
remain
poorly
understood.
Here
we
show
that
tumors
induce
de
novo
steroidogenesis
in
T
lymphocytes
anti-tumor
immunity.
Using
a
transgenic
steroidogenesis-reporter
mouse
line
identify
and
characterize
steroidogenic
cells,
defining
global
gene
expression
identity
of
these
steroid-producing
cells
regulatory
networks
by
using
single-cell
transcriptomics.
Genetic
ablation
restricts
primary
tumor
growth
metastatic
dissemination
models.
Steroidogenic
dysregulate
immunity,
inhibition
pathway
is
sufficient
restore
This
study
demonstrates
as
mechanism
immunosuppression
potential
druggable
target.