International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(2), P. 1526 - 1526
Published: Jan. 12, 2023
Inflammatory
bowel
disease
(IBD),
comprising
Crohn’s
(CD)
and
ulcerative
colitis
(UC),
is
a
heterogeneous
state
of
chronic
intestinal
inflammation
with
no
exact
known
cause.
Intestinal
innate
immunity
enacted
by
neutrophils,
monocytes,
macrophages,
dendritic
cells
(DCs),
lymphoid
NK
cells,
characterized
their
capacity
to
produce
rapid
nonspecific
reaction
as
first-line
response.
Innate
immune
(IIC)
defend
against
pathogens
excessive
entry
microorganisms,
while
preserving
tolerance
resident
microbiota.
Changes
this
equilibrium
are
linked
in
the
gut
IBD.
IICs
mediate
host
defense
responses,
inflammation,
tissue
healing
producing
cytokines
chemokines,
activating
complement
cascade
phagocytosis,
or
presenting
antigens
activate
adaptive
exert
important
functions
that
promote
ameliorate
cellular
molecular
mechanisms
underlie
sustain
A
comprehensive
understanding
underlying
these
clinical
manifestations
will
be
for
developing
therapies
targeting
system
IBD
patients.
This
review
examines
complex
roles
interactions
among
IICs,
other
non-immune
homeostasis
pathological
conditions.
Frontiers in Immunology,
Journal Year:
2019,
Volume and Issue:
10
Published: March 11, 2019
Ulcerative
colitis
(UC)
and
Crohn's
disease
(CD),
collectively
known
as
Inflammatory
Bowel
Diseases
(IBD),
are
caused
by
a
complex
interplay
between
genetic,
immunologic,
microbial
environmental
factors.
Dysbiosis
of
the
gut
microbiome
is
increasingly
considered
to
be
causatively
related
IBD
strongly
affected
components
Western
life
style.
Bacteria
that
ferment
fibers
produce
short
chain
fatty
acids
(SCFAs)
typically
reduced
in
mucosa
feces
patients
with
IBD,
compared
healthy
individuals.
SCFAs,
such
acetate,
propionate
butyrate,
important
metabolites
maintaining
intestinal
homeostasis.
Several
studies
have
indeed
shown
fecal
SCFAs
levels
active
IBD.
an
fuel
for
epithelial
cells
strengthen
barrier
function.
Recent
findings,
however,
show
particular
also
immunomodulatory
functions.
Absorption
facilitated
substrate
transporters
like
MCT1
SMCT1
promote
cellular
metabolism.
Moreover,
may
signal
through
cell
surface
G-protein
coupled
receptors
(GPCRs),
GPR41,
GPR43,
GPR109A,
activate
signaling
cascades
control
immune
Transgenic
mouse
models
support
key
role
these
GPCRs
controlling
inflammation.
Here,
we
present
overview
production
their
effects
on
specific
emphasis
relevance
discuss
therapeutic
potential
either
applied
directly
or
stimulating
SCFAs-producing
bacteria
pre-
probiotic
approaches.
Physiological Reviews,
Journal Year:
2019,
Volume and Issue:
99(3), P. 1325 - 1380
Published: March 28, 2019
Sleep
and
immunity
are
bidirectionally
linked.
Immune
system
activation
alters
sleep,
sleep
in
turn
affects
the
innate
adaptive
arm
of
our
body’s
defense
system.
Stimulation
immune
by
microbial
challenges
triggers
an
inflammatory
response,
which,
depending
on
its
magnitude
time
course,
can
induce
increase
duration
intensity,
but
also
a
disruption
sleep.
Enhancement
during
infection
is
assumed
to
feedback
promote
host
defense.
Indeed,
various
parameters,
associated
with
reduced
risk,
improve
outcome
vaccination
responses.
The
induction
hormonal
constellation
that
supports
functions
one
likely
mechanism
underlying
immune-supporting
effects
In
absence
infectious
challenge,
appears
homeostasis
through
several
mediators,
such
as
cytokines.
This
notion
supported
findings
prolonged
deficiency
(e.g.,
short
duration,
disturbance)
lead
chronic,
systemic
low-grade
inflammation
diseases
have
component,
like
diabetes,
atherosclerosis,
neurodegeneration.
Here,
we
review
available
data
this
regulatory
sleep-immune
crosstalk,
point
out
methodological
challenges,
suggest
questions
open
for
future
research.
Science,
Journal Year:
2017,
Volume and Issue:
357(6349)
Published: July 27, 2017
Kynurenine
metabolites
are
generated
by
tryptophan
catabolism
and
regulate
biological
processes
that
include
host-microbiome
signaling,
immune
cell
response,
neuronal
excitability.
Enzymes
of
the
kynurenine
pathway
expressed
in
different
tissues
types
throughout
body
regulated
cues,
including
nutritional
inflammatory
signals.
As
a
consequence
this
systemic
metabolic
integration,
peripheral
inflammation
can
contribute
to
accumulation
brain,
which
has
been
associated
with
depression
schizophrenia.
Conversely,
be
suppressed
activating
clearance
exercised
skeletal
muscle.
The
effect
exercise
training
on
through
modulation
highlights
an
important
mechanism
interorgan
cross-talk
mediated
these
metabolites.
Here,
we
discuss
mechanisms
tryptophan-kynurenine
metabolism
their
effects
inflammatory,
metabolic,
oncologic,
psychiatric
disorders.
