International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(18), P. 9776 - 9776
Published: Sept. 10, 2024
Changes
in
maternal
gut
microbiota
due
to
stress
and/or
ethanol
exposure
can
have
lasting
effects
on
offspring’s
health,
particularly
regarding
immunity,
inflammation
response,
and
susceptibility
psychiatric
disorders.
The
literature
search
for
this
review
was
conducted
using
PubMed
Scopus,
employing
keywords
phrases
related
stress,
exposure,
microbiota,
microbiome,
gut–brain
axis,
diet,
dysbiosis,
progesterone,
placenta,
prenatal
development,
inflammation,
depression
identify
relevant
studies
both
preclinical
human
research.
Only
a
limited
number
of
reviews
were
included
support
the
arguments.
encompassed
from
1990s
present.
This
begins
by
exploring
role
modulating
host
health
disease.
It
then
examines
how
disturbances
affect
immune
system.
analysis
continues
investigating
interplay
between
focusing
influences
offspring
its
implications
depression.
also
considers
impact
consumption
with
an
emphasis
microbiota.
Finally,
it
is
suggested
that
dysbiosis
may
be
significantly
exacerbated
combined
leading
system
dysfunction
chronic
which
could
increase
risk
offspring.
These
interactions
underscore
potential
novel
mental
interventions
address
especially
relation
health.
Frontiers in Psychiatry,
Journal Year:
2024,
Volume and Issue:
15
Published: Feb. 9, 2024
Depression
is
considered
a
multifaceted
and
intricate
mental
disorder
of
growing
concern
due
to
its
significant
impact
on
global
health
issues.
The
human
gut
microbiota,
also
known
as
the
“second
brain,”
has
an
important
role
in
CNS
by
regulating
it
through
chemical,
immunological,
hormonal,
neurological
processes.
Various
studies
have
found
bidirectional
link
between
brain
gut,
emphasizing
onset
depression
therapies.
biological
molecular
processes
underlying
microbiota
are
required,
association
may
represent
novel
study.
However,
profound
insights
into
stratification
diversity
still
uncommon.
This
article
investigates
emerging
evidence
bacterial
relationship
brain’s
system
potential
pathogenicity
relevance.
interplay
immune
system,
nervous
neurotransmitter
synthesis,
neuroplasticity
transitions
widely
studied.
consequences
stress,
dietary
fibers,
probiotics,
prebiotics,
antibiotics
GB
axis
being
Multiple
revealed
this
led
development
effective
microbiota-based
drugs
for
both
prevention
treatment.
Therefore,
results
support
hypothesis
that
influences
provide
promising
area
research
improved
knowledge
etiology
disease
future
Journal of Advanced Research,
Journal Year:
2023,
Volume and Issue:
64, P. 171 - 181
Published: Nov. 13, 2023
Immune-inflammatory
pathways
in
major
depressive
disorder
are
confined
to
the
dysmood
(MDMD)
phenotype
(Maes
et
al.,
2022).
No
studies
have
addressed
immune
profile
of
first
episode
MDMD
(FE-MDMD).
Frontiers in Psychiatry,
Journal Year:
2023,
Volume and Issue:
14
Published: April 26, 2023
Neuroticism,
a
personality
trait,
can
predict
major
depressive
disorder
(MDD).
The
current
study
aims
to
determine
whether
a)
neuroticism
is
feature
of
the
acute
state
MDD,
including
suicidal
behaviors
(SB);
and
b)
adverse
childhood
experiences
(ACEs)
are
associated
with
in
MDD.
Brain Sciences,
Journal Year:
2023,
Volume and Issue:
13(7), P. 1090 - 1090
Published: July 18, 2023
Major
depressive
disorder
(MDD)
and
its
severe
subtype,
major
dysmood
(MDMD),
are
distinguished
by
activation
of
inflammatory
growth
factor
subnetworks,
which
associated
with
recurrence
illness
(ROI)
adverse
childhood
experiences
(ACEs).
Nerve
(NGF)
plays
a
crucial
role
in
facilitating
neuro-immune
communications
may
regulate
the
response.
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: April 17, 2023
Abstract
Background
Immune-inflammatory
pathways
in
major
depressive
disorder
are
confined
to
the
dysmood
(MDMD)
phenotype
(Maes
et
al.,
2022).
No
studies
have
addressed
immune
profile
of
first
episode
MDMD
(FE-MDMD).
Methods
This
study
examines
48
cytokines/chemokines/growth
factors,
and
classical
M1,
alternative
M2,
T
helper
(Th)-1,
Th-2,
Th-17
phenotypes,
immune-inflammatory
response
system
(IRS),
compensatory
immunoregulatory
(CIRS),
neuro-immunotoxicity
profiles
acute
phase
FE-MDMD
(n=71)
versus
healthy
controls
(40).
Results
patients
show
significantly
activated
Th-1,
IRS,
CIRS,
neurotoxicity,
but
not
Th-2
or
Th-17,
compared
controls.
is
accompanied
by
Th-1
polarization,
while
there
no
changes
M1/M2
IRS/CIRS
ratios.
The
top
single
indicator
was
far
interleukin
(IL)-16,
followed
at
a
distance
TRAIL,
IL-2R,
tumor
necrosis
factor
(TNF)-β.
severity
depression
anxiety
strongly
associated
with
IRS
(positively)
(inversely)
profiles,
whereas
suicidal
behavior
M1
activation.
Around
56-60%
variance
depression,
anxiety,
scores
explained
IL-16,
platelet-derived
growth
(PDGF)
(both
positively),
IL-1
receptor
antagonist
(inversely).
Increased
neurotoxicity
mainly
driven
TNF-α,
IL-6
chemokine
(CCL2,
CCL11,
CXCL1,
CXCL10)
signaling.
Antidepressant-treated
an
increased
ratio
as
drug-naïve
patients.
Conclusions
positive
regulation
polarization
cell
activation
(via
binding
IL-16
CD4),
TNF,
chemokine,
Cells,
Journal Year:
2023,
Volume and Issue:
12(9), P. 1237 - 1237
Published: April 25, 2023
Although
previously
restricted
to
a
limited
number
of
medical
conditions,
there
is
growing
appreciation
that
'autoimmune'
(or
immune-mediated)
processes
are
important
aspects
wide
array
diverse
including
cancers,
neurodegenerative
diseases
and
psychiatric
disorders.
All
these
classes
conditions
associated
with
alterations
in
mitochondrial
function
across
an
cell
types.
Accumulating
data
indicate
the
presence
melatonergic
pathway
possibly
all
body
cells,
consequences
for
pathways
crucial
driving
CD8+
T
B-cell
'autoimmune'-linked
processes.
Melatonin
suppression
coupled
upregulation
oxidative
stress
suppress
PTEN-induced
kinase
1
(PINK1)/parkin-driven
mitophagy,
raising
levels
major
histocompatibility
complex
(MHC)-1,
which
underpins
chemoattraction
cells
activation
antibody-producing
B-cells.
Many
factors
closely
autoimmunity,
gut
microbiome/permeability,
circadian
rhythms,
aging,
aryl
hydrocarbon
receptor,
brain-derived
neurotrophic
factor
(BDNF)
its
receptor
tyrosine
B
(TrkB)
interact
pathway.
A
future
research
directions
novel
treatment
implications
indicated
this
collection
poorly
conceptualized
treated
presentations.
It
proposed
etiology
many
'autoimmune'/'immune-mediated'
disorders
should
be
as
significantly
determined
by
dysregulation,
being
aspect
pathoetiologies.
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: March 28, 2024
Abstract
Major
depressive
disorder
(MDD)
is
accompanied
by
activated
neuro-immune
pathways,
increased
physiosomatic
and
chronic
fatigue-fibromyalgia
(FF)
symptoms.
The
most
severe
MDD
phenotype,
namely
major
dysmood
(MDMD),
associated
with
adverse
childhood
experiences
(ACEs)
negative
life
events
(NLEs)
which
induce
cytokines/chemokines/growth
factors.
To
delineate
the
impact
of
ACE
+
NLEs
on
FF
symptoms
in
first
episode
(FE)-MDMD,
examine
whether
these
effects
are
mediated
immune
profiles.
ACEs,
NLEs,
symptoms,
48
factors
were
measured
64
FE-MDMD
patients
32
normal
controls.
Physiosomatic,
gastro-intestinal
belong
to
same
factor
as
depression,
anxiety,
melancholia,
insomnia.
extracted
from
seven
domains
labeled
physio-affective
phenome
depression.
A
part
(59.0%)
variance
explained
independent
interleukin
(IL)-16
IL-8
(positively),
CCL3
IL-1
receptor
antagonist
(inversely
correlated).
(46.5%)
(IL)-16,
TNF-related
apoptosis-inducing
ligand
(TRAIL)
(positively)
combined
activities
immunoregulatory
cytokines
associated).
Partial
least
squares
analysis
shows
that
exert
a
substantial
influence
partly
an
network
composed
interleukin-16,
CCL27,
TRAIL,
macrophage-colony
stimulating
factor,
stem
cell
growth
factor.
caused
immune-associated
neurotoxicity
due
T
helper
(Th)-1
polarization
M1
macrophage
activation
relative
lowered
compensatory
protection.
medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: June 13, 2023
Abstract
Background
Major
depressive
disorder
(MDD)
is
characterized
by
increased
T
helper
(Th)1
polarization,
cell
activation
(e.g.,
CD71+
and
CD40L+),
cannabinoid
receptor
type
2
bearing
CD20+
B
cells;
lower
regulatory
(Treg)
numbers.
Aims
To
delineate
the
effects
of
adverse
childhood
experiences
(ACEs)
recurrence
illness
(ROI)
on
activated
CB2-bearing
populations,
Tregs,
including
FoxP3+CD152+,
FoxP3+GARP+,
FoxP3+CB1+
cells.
Methods
We
measured
ROI,
ACEs,
number
cells,
CD20+CB2+
in
30
MDD
patients
20
healthy
controls.
Results
A
larger
part
variance
depression
phenome
(40.8%)
was
explained
lowered
Tregs.
ROI
lifetime
suicidal
behaviors
were
significantly
positively
associated
with
CD20+CB2+,
CD3+CD71+,
CD3+CD40L+,
CD4+CD71+,
CD4+CD40L+,
CD4HLADR+
correlated
CD8+CD40L+
The
sum
ACEs
CD4+40L+
numbers,
(positively)
Treg
(inversely)
indices.
One
replicable
latent
vector
could
be
extracted
from
current
behaviors,
episodes,
severity
depression,
48.8%
its
ACEs.
Conclusions
ACE-induced
effector
cytotoxic
cells
autoimmune
potential,
coupled
numbers
are
a
key
component
depression.
findings
indicate
that
increasing
caused
processes,
which
consequence
sensitization
immune
responses.