Journal of Clinical Investigation,
Journal Year:
2021,
Volume and Issue:
131(12)
Published: June 14, 2021
Traumatic
brain
injury
(TBI)
is
a
chronic
and
progressive
disease,
management
requires
an
understanding
of
both
the
primary
neurological
secondary
sequelae
that
affect
peripheral
organs,
including
gastrointestinal
(GI)
tract.
The
brain-gut
axis
composed
bidirectional
pathways
through
which
TBI-induced
neuroinflammation
neurodegeneration
impact
gut
function.
resulting
dysautonomia
systemic
inflammation
contribute
to
GI
events,
dysmotility
increased
mucosal
permeability.
These
effects
shape,
are
shaped
by,
changes
in
microbiota
composition
activation
resident
recruited
immune
cells.
Microbial
products
cell
mediators
turn
modulate
activity.
Importantly,
enteric
inflammatory
challenges
prolong
worsen
neuropathology
neurobehavioral
deficits.
importance
communication
maintaining
homeostasis
highlights
it
as
viable
therapeutic
target
for
TBI.
Currently,
treatments
directed
toward
dysautonomia,
dysbiosis,
and/or
offer
most
promise.
Journal of Neurogastroenterology and Motility,
Journal Year:
2020,
Volume and Issue:
27(1), P. 19 - 34
Published: Nov. 9, 2020
Of
all
microorganisms
in
the
human
body,
largest
and
most
complex
population
resides
gastrointestinal
(GI)
tract.
The
gut
microbiota
continuously
adapts
to
host
environment
serves
multiple
critical
functions
for
their
hosts,
including
regulating
immunity,
procuring
energy
from
food,
preventing
colonization
of
pathogens.
Mounting
evidence
has
suggested
microbial
imbalance
(dysbiosis)
as
a
core
pathophysiology
development
GI
motility
metabolic
disorders,
such
irritable
bowel
syndrome
diabetes.
Current
research
focused
on
discovering
associations
between
these
disorders
dysbiosis;
however,
whether
are
consequence
or
cause
is
still
mostly
unexplored.
State-of-the-art
studies
have
investigated
how
microbes
communicate
with
our
body
systems
through
microbiota-derived
metabolites
they
able
modulate
physiology.
There
now
mounting
that
alterations
composition
small
intestinal
an
association
dysmotility
disorders.
Although
treatment
options
dysbiosis
currently
limited,
antibiotics,
fecal
transplantation,
probiotics,
dietary
interventions
best
options.
However,
broad-spectrum
antibiotics
been
viewed
skepticism
due
risk
developing
antibiotic
resistant
bacteria.
Studies
warranted
elucidate
cellular
molecular
pathways
underlying
microbiota-host
crosstalk
powerful
platform
future
therapeutic
approaches.
Here,
we
review
recent
literature
and/or
interactions
involved
Oxidative Medicine and Cellular Longevity,
Journal Year:
2019,
Volume and Issue:
2019, P. 1 - 10
Published: April 17, 2019
Gut
microbiota
consists
of
over
100
trillion
microorganisms
including
at
least
1000
different
species
bacteria
and
is
crucially
involved
in
physiological
pathophysiological
processes
occurring
the
host.
An
imbalanced
gastrointestinal
ecosystem
(dysbiosis)
seems
to
be
a
contributor
development
maintenance
several
diseases,
such
as
Alzheimer’s
disease,
depression,
type
2
diabetes
mellitus.
Interestingly,
three
disorders
are
frequently
associated
demonstrated
by
high
comorbidity
rates.
In
this
review,
we
introduce
gut
its
role
both
normal
pathological
processes;
then,
discuss
importance
gut-brain
axis
well
oxidative
stress
inflammation
mediators
which
dysbiosis
involved.
Specific
sections
pertain
altered
pathogenesis
The
therapeutic
implications
manipulation
briefly
discussed.
Finally,
conclusion
comments
on
possible
common
pathogenetic
(via
inflammation)
shared
disorders.
Acta Neuropathologica,
Journal Year:
2019,
Volume and Issue:
138(6), P. 987 - 1012
Published: July 30, 2019
Microglia
are
highly
plastic
immune
cells
which
exist
in
a
continuum
of
activation
states.
By
shaping
the
function
oligodendrocyte
precursor
(OPCs),
brain
differentiate
to
myelin-forming
cells,
microglia
participate
both
myelin
injury
and
remyelination
during
multiple
sclerosis.
However,
mode(s)
action
supporting
or
inhibiting
repair
is
still
largely
unclear.
Here,
we
analysed
effects
extracellular
vesicles
(EVs)
produced
vitro
by
either
pro-inflammatory
pro-regenerative
on
OPCs
at
demyelinated
lesions
caused
lysolecithin
injection
mouse
corpus
callosum.
Immunolabelling
for
proteins
electron
microscopy
showed
that
EVs
released
blocked
remyelination,
whereas
co-cultured
with
immunosuppressive
mesenchymal
stem
promoted
OPC
recruitment
repair.
The
molecular
mechanisms
responsible
harmful
beneficial
EV
actions
were
dissected
primary
cultures.
exposing
OPCs,
cultured
alone
astrocytes,
inflammatory
EVs,
observed
blockade
maturation
only
presence
implicating
these
failure.
Biochemical
fractionation
revealed
astrocytes
may
be
converted
into
cargo,
as
indicated
immunohistochemical
qPCR
analyses,
surface
lipid
components
promote
migration
and/or
differentiation,
linking
lipids
Although
through
species
enhance
remain
fully
defined,
provide
first
demonstration
vesicular
sphingosine
1
phosphate
stimulates
migration,
fundamental
step
From
this
study,
microglial
emerge
multimodal
multitarget
signalling
mediators
able
influence
around
lesions,
exploited
develop
novel
approaches
not
sclerosis,
but
also
neurological
neuropsychiatric
diseases
characterized
demyelination.
Journal of Clinical Investigation,
Journal Year:
2021,
Volume and Issue:
131(12)
Published: June 14, 2021
Traumatic
brain
injury
(TBI)
is
a
chronic
and
progressive
disease,
management
requires
an
understanding
of
both
the
primary
neurological
secondary
sequelae
that
affect
peripheral
organs,
including
gastrointestinal
(GI)
tract.
The
brain-gut
axis
composed
bidirectional
pathways
through
which
TBI-induced
neuroinflammation
neurodegeneration
impact
gut
function.
resulting
dysautonomia
systemic
inflammation
contribute
to
GI
events,
dysmotility
increased
mucosal
permeability.
These
effects
shape,
are
shaped
by,
changes
in
microbiota
composition
activation
resident
recruited
immune
cells.
Microbial
products
cell
mediators
turn
modulate
activity.
Importantly,
enteric
inflammatory
challenges
prolong
worsen
neuropathology
neurobehavioral
deficits.
importance
communication
maintaining
homeostasis
highlights
it
as
viable
therapeutic
target
for
TBI.
Currently,
treatments
directed
toward
dysautonomia,
dysbiosis,
and/or
offer
most
promise.