Science,
Journal Year:
2017,
Volume and Issue:
356(6342), P. 1026 - 1030
Published: June 9, 2017
Tissue
repair
after
injury
is
a
complex,
metabolically
demanding
process.
Depending
on
the
tissue’s
regenerative
capacity
and
quality
of
inflammatory
response,
outcome
generally
imperfect,
with
some
degree
fibrosis,
which
defined
by
aberrant
accumulation
collagenous
connective
tissue.
Inflammatory
cells
multitask
at
wound
site
facilitating
debridement
producing
chemokines,
metabolites,
growth
factors.
If
this
well-orchestrated
response
becomes
dysregulated,
can
become
chronic
or
progressively
fibrotic,
both
outcomes
impairing
tissue
function,
ultimately
lead
to
organ
failure
death.
Here
we
review
current
understanding
role
inflammation
cell
metabolism
in
tissue-regenerative
responses,
highlight
emerging
concepts
that
may
expand
therapeutic
perspectives,
briefly
discuss
where
important
knowledge
gaps
remain.
Frontiers in Immunology,
Journal Year:
2014,
Volume and Issue:
5
Published: Oct. 17, 2014
Studies
on
monocyte
and
macrophage
biology
differentiation
have
revealed
the
pleiotropic
activities
of
these
cells.
Macrophages
are
tissue
sentinels
that
maintain
integrity
by
eliminating/repairing
damaged
cells
matrices.
In
this
M2-like
mode
they
can
also
promote
tumor
growth.
Conversely,
M1-like
macrophages
key
effector
for
elimination
pathogens,
virally
infected,
cancer
Macrophage
from
monocytes
occurs
in
concomitance
with
acquisition
a
functional
phenotype
depends
microenvironmental
signals,
thereby
accounting
many
apparently
opposed
functions.
Many
questions
arise.
When
differentiate
into
(concomitantly
adopting
specific
program,
M1
or
M2),
do
all
die
during
inflammatory
reaction,
some
them
survive?
Do
those
survive
become
quiescent
macrophages,
able
to
react
as
naïve
new
challenge?
Or,
monocyte-derived
conserve
“memory”
their
past
activation?
This
review
will
address
important
under
general
framework
role
initiation,
development,
resolution
chronicization
inflammation.
British Journal of Pharmacology,
Journal Year:
2015,
Volume and Issue:
173(4), P. 649 - 665
Published: March 20, 2015
Microglia
are
critical
nervous
system‐specific
immune
cells
serving
as
tissue‐resident
macrophages
influencing
brain
development,
maintenance
of
the
neural
environment,
response
to
injury
and
repair.
As
influenced
by
their
microglia
assume
a
diversity
phenotypes
retain
capability
shift
functions
maintain
tissue
homeostasis.
In
comparison
with
peripheral
macrophages,
demonstrate
similar
unique
features
regards
phenotype
polarization,
allowing
for
innate
immunological
functions.
can
be
stimulated
LPS
or
IFN
‐
γ
an
M
1
expression
pro‐inflammatory
cytokines
IL‐4/IL‐13
2
resolution
inflammation
Increasing
evidence
suggests
role
metabolic
reprogramming
in
regulation
inflammatory
response.
Studies
using
that
polarization
is
often
accompanied
from
oxidative
phosphorylation
aerobic
glycolysis
energy
production.
More
recently,
link
between
mitochondrial
metabolism
has
been
considered
microglia.
Under
these
conditions,
demands
would
associated
functional
activities
cell
survival
thus,
may
serve
influence
contribution
activation
various
neurodegenerative
conditions.
This
review
examines
states
relationship
metabolism.
Additional
supporting
experimental
data
provided
shifts
primary
BV
‐2
line
induced
under
(
M1
)
IL
‐4/
IL‐13
M2
polarization.
Linked
Articles
article
part
themed
section
on
Inflammation:
maladies,
models,
mechanisms
molecules.
To
view
other
articles
this
visit
http://dx.doi.org/10.1111/bph.2016.173.issue-4
Cancers,
Journal Year:
2014,
Volume and Issue:
6(3), P. 1670 - 1690
Published: Aug. 13, 2014
During
tumor
progression,
circulating
monocytes
and
macrophages
are
actively
recruited
into
tumors
where
they
alter
the
microenvironment
to
accelerate
progression.
Macrophages
shift
their
functional
phenotypes
in
response
various
microenvironmental
signals
generated
from
stromal
cells.
Based
on
function,
divided
broadly
two
categories:
classical
M1
alternative
M2
macrophages.
The
macrophage
is
involved
inflammatory
response,
pathogen
clearance,
antitumor
immunity.
In
contrast,
influences
an
anti-inflammatory
wound
healing,
pro-tumorigenic
properties.
Tumor-associated
(TAMs)
closely
resemble
M2-polarized
critical
modulators
of
microenvironment.
Clinicopathological
studies
have
suggested
that
TAM
accumulation
correlates
with
a
poor
clinical
outcome.
Consistent
evidence,
experimental
animal
supported
notion
TAMs
can
provide
favorable
promote
development
this
review
article,
we
present
overview
mechanisms
responsible
for
recruitment
highlight
roles
regulation
angiogenesis,
invasion,
metastasis,
immunosuppression,
chemotherapeutic
resistance.
Finally,
discuss
TAM-targeting
therapy
as
promising
novel
strategy
indirect
cancer
therapy.
Nutrients,
Journal Year:
2018,
Volume and Issue:
10(11), P. 1618 - 1618
Published: Nov. 2, 2018
This
review
offers
a
systematic
understanding
about
how
polyphenols
target
multiple
inflammatory
components
and
lead
to
anti-inflammatory
mechanisms.
It
provides
clear
of
the
molecular
mechanisms
action
phenolic
compounds.
Polyphenols
regulate
immunity
by
interfering
with
immune
cell
regulation,
proinflammatory
cytokines’
synthesis,
gene
expression.
They
inactivate
NF-κB
(nuclear
factor
kappa-light-chain-enhancer
activated
B
cells)
modulate
mitogen-activated
protein
Kinase
(MAPk)
arachidonic
acids
pathways.
Polyphenolic
compounds
inhibit
phosphatidylinositide
3-kinases/protein
kinase
(PI3K/AkT),
inhibitor
kappa
kinase/c-Jun
amino-terminal
kinases
(IKK/JNK),
mammalian
rapamycin
complex
1
(mTORC1)
which
is
that
controls
JAK/STAT.
can
suppress
toll-like
receptor
(TLR)
pro-inflammatory
genes’
Their
antioxidant
activity
ability
enzymes
involved
in
production
eicosanoids
contribute
as
well
their
anti-inflammation
properties.
certain
reactive
oxygen
species
ROS
like
xanthine
oxidase
NADPH
(NOX)
while
they
upregulate
other
endogenous
superoxide
dismutase
(SOD),
catalase,
glutathione
(GSH)
peroxidase
(Px).
Furthermore,
phospholipase
A2
(PLA2),
cyclooxygenase
(COX)
lipoxygenase
(LOX)
leading
reduction
prostaglandins
(PGs)
leukotrienes
(LTs)
inflammation
antagonism.
The
effects
these
biologically
active
on
system
are
associated
extended
health
benefits
for
different
chronic
diseases.
Studies
plant
extracts
show
play
beneficial
role
prevention
progress
diseases
related
such
diabetes,
obesity,
neurodegeneration,
cancers,
cardiovascular
diseases,
among
conditions.
Science,
Journal Year:
2014,
Volume and Issue:
344(6186), P. 921 - 925
Published: May 9, 2014
Long
recognized
as
an
evolutionarily
ancient
cell
type
involved
in
tissue
homeostasis
and
immune
defense
against
pathogens,
macrophages
are
being
rediscovered
regulators
of
several
diseases,
including
cancer.
Here
we
show
that
mice,
mammary
tumor
growth
induces
the
accumulation
tumor-associated
(TAMs)
phenotypically
functionally
distinct
from
(MTMs).
TAMs
express
adhesion
molecule
Vcam1
proliferate
upon
their
differentiation
inflammatory
monocytes,
but
do
not
exhibit
“alternatively
activated”
phenotype.
TAM
terminal
depends
on
transcriptional
regulator
Notch
signaling,
RBPJ;
TAM,
MTM,
depletion
restores
tumor-infiltrating
cytotoxic
T
responses
suppresses
growth.
These
findings
reveal
ontogeny
a
discrete
tumor-elicited
response,
which
may
provide
new
opportunities
for
cancer
immunotherapy.
Frontiers in Physiology,
Journal Year:
2018,
Volume and Issue:
9
Published: May 1, 2018
Macrophages
play
key
roles
in
all
phases
of
adult
wound
healing,
which
are
inflammation,
proliferation
and
remodeling.
As
wounds
heal,
the
local
macrophage
population
transitions
from
predominantly
pro-inflammatory
(M1-like
phenotypes)
to
anti-inflammatory
(M2-like
phenotypes).
Non-healing
chronic
wounds,
such
as
pressure,
arterial,
venous
diabetic
ulcers
indefinitely
remain
inflammation—the
first
stage
healing.
Thus,
macrophages
retain
characteristics.
This
review
discusses
physiology
monocytes
acute
healing
different
phenotypes
described
literature
for
both
vitro
vivo
models.
We
also
discuss
aberrations
that
occur
populations
attempts
restore
function
by
therapeutic
approaches.
These
include
endogenous
M1
attenuation,
exogenous
M2
supplementation
modulation/M2
promotion
via
mesenchymal
stem
cells,
growth
factors,
biomaterials,
heme
oxygenase-1
(HO-1)
expression
oxygen
therapy.
recognize
challenges
controversies
exist
this
field,
standardization
phenotype
nomenclature,
definition
their
distinct
understanding
is
optimal
order
promote
wounds.
International Journal of Molecular Sciences,
Journal Year:
2018,
Volume and Issue:
19(6), P. 1801 - 1801
Published: June 19, 2018
Experimental
models
have
often
been
at
the
origin
of
immunological
paradigms
such
as
M1/M2
dichotomy
following
macrophage
polarization.
However,
this
clear
in
animal
is
not
obvious
humans,
and
separating
line
between
M1-like
M2-like
macrophages
rather
represented
by
a
continuum,
where
boundaries
are
still
unclear.
Indeed,
human
infectious
diseases,
characterized
either
back
forth
or
mixed
profile
pro-inflammatory
microenvironment
(dominated
interleukin
(IL)-1β,
IL-6,
IL-12,
IL-23
Tumor
Necrosis
Factor
(TNF)-α
cytokines)
tissue
injury
driven
classically
activated
(M1-like)
wound
healing
alternatively
(M2-like)
an
anti-inflammatory
environment
IL-10,
Transforming
growth
factor
(TGF)-β,
chemokine
ligand
(CCL)1,
CCL2,
CCL17,
CCL18,
CCL22).
This
review
brews
complexity
situation
during
diseases
stressing
on
continuum
extremes.
We
first
discuss
basic
biology
polarization,
function,
role
inflammatory
process
its
resolution.
Secondly,
we
relevance
polarization
neglected
possibility
to
interfere
with
activation
states
promising
therapeutic
strategy
treatment
diseases.