Expert Review of Clinical Immunology,
Journal Year:
2019,
Volume and Issue:
15(12), P. 1287 - 1302
Published: Nov. 1, 2019
Introduction:
The
development
of
childhood
asthma
is
caused
by
a
combination
genetic
factors
and
environmental
exposures.
Epigenetics
describes
mechanisms
(heritable)
regulation
gene
expression
that
occur
without
changes
in
DNA
sequence.
strongly
related
to
aging,
cell-type
specific,
includes
methylation,
noncoding
RNAs,
histone
modifications.Areas
covered:
This
review
summarizes
recent
epigenetic
studies
humans,
which
mostly
involve
methylation
published
the
five
years.
Environmental
exposures,
particular
cigarette
smoking,
have
significant
impact
on
changes,
but
few
these
signals
are
also
associated
with
asthma.
Several
asthma-associated
variants
relate
methylation.
Epigenetic
can
be
better
understood
studying
their
correlation
expression,
revealed
higher
presence
activation
blood
eosinophils
Strong
associations
nasal
signatures
atopic
were
identified,
replicable
across
different
populations.Expert
commentary:
markers
been
asthma,
might
serve
as
biomarker
causal
longitudinal
relationships
between
epigenetics
disease,
exposures
need
further
investigated.
Efforts
should
made
understand
cell-type-specific
Allergy,
Journal Year:
2021,
Volume and Issue:
76(12), P. 3659 - 3686
Published: Sept. 14, 2021
During
the
past
years,
there
has
been
a
global
outbreak
of
allergic
diseases,
presenting
considerable
medical
and
socioeconomical
burden.
A
large
fraction
diseases
is
characterized
by
type
2
immune
response
involving
Th2
cells,
innate
lymphoid
eosinophils,
mast
M2
macrophages.
Biomarkers
are
valuable
parameters
for
precision
medicine
as
they
provide
information
on
disease
endotypes,
clusters,
diagnoses,
identification
therapeutic
targets,
monitoring
treatment
efficacies.
The
availability
powerful
omics
technologies,
together
with
integrated
data
analysis
network-based
approaches
can
help
clinically
useful
biomarkers.
These
biomarkers
need
to
be
accurately
quantified
using
robust
reproducible
methods,
such
reliable
point-of-care
systems.
Ideally,
samples
should
collected
quick,
cost-efficient
noninvasive
methods.
In
recent
plethora
research
directed
toward
finding
novel
diseases.
Promising
include
sputum
serum
periostin
exhaled
nitric
oxide.
Several
other
biomarkers,
pro-inflammatory
mediators,
miRNAs,
eicosanoid
molecules,
epithelial
barrier
integrity,
microbiota
changes
diagnosis
in
serum,
body
fluids
air.
Herein,
we
review
studies
asthma,
chronic
urticaria,
atopic
dermatitis,
rhinitis,
rhinosinusitis,
food
allergies,
anaphylaxis,
drug
hypersensitivity
allergen
immunotherapy.
addition,
discuss
COVID-19
within
perspective
recommendations
management
asthmatic
patients
during
pandemic.
Cells,
Journal Year:
2022,
Volume and Issue:
11(17), P. 2764 - 2764
Published: Sept. 5, 2022
Asthma
is
a
heterogeneous
lung
disease
with
variable
phenotypes
(clinical
presentations)
and
distinctive
endotypes
(mechanisms).
Over
the
last
decade,
considerable
efforts
have
been
made
to
dissect
cellular
molecular
mechanisms
of
asthma.
Aberrant
T
helper
type
2
(Th2)
inflammation
most
important
pathological
process
for
asthma,
which
mediated
by
Th2
cytokines,
such
as
interleukin
(IL)-5,
IL-4,
IL-13.
Approximately
50%
mild-to-moderate
asthma
large
portion
severe
induced
Th2-dependent
inflammation.
Th2-low
can
be
non-Th2
including
IL-17
tumor
necrosis
factor-α.
There
emerging
evidence
demonstrate
that
inflammation-independent
processes
also
contribute
pathogenesis.
Protein
kinases,
adapter
protein,
microRNAs,
ORMDL3,
gasdermin
B
are
newly
identified
molecules
drive
progression,
independent
Eosinophils,
IgE,
fractional
exhaled
nitric
oxide,
periostin
practical
biomarkers
Th2-high
Sputum
neutrophils
easily
used
diagnose
Despite
progress,
more
studies
needed
delineate
complex
identify
new
better
diagnosis,
classification,
treatment.
Journal of Clinical Medicine,
Journal Year:
2021,
Volume and Issue:
10(2), P. 169 - 169
Published: Jan. 6, 2021
Asthma
and
obesity
are
two
epidemics
affecting
the
developed
world.
The
relationship
between
both
asthma
severe
appears
to
be
weight-dependent,
causal,
partly
genetic,
probably
bidirectional.
There
distinct
phenotypes:
1.
Allergic
in
children
with
obesity,
which
worsens
a
pre-existing
asthma,
2.
An
often
non
allergic,
late-onset
developing
as
consequence
of
obesity.
In
infiltration
adipose
tissue
by
macrophages
M1,
together
an
increased
expression
multiple
mediators
that
amplify
propagate
inflammation,
is
considered
culprit
obesity-related
inflammation.
Adipose
important
source
adipokines,
such
pro-inflammatory
leptin,
produced
excess
adiponectin
anti-inflammatory
effects
reduced
synthesis.
inflammatory
process
also
involves
synthesis
cytokines
IL-1β,
IL-6,
TNFα,
TGFβ,
contribute
pathogenesis.
contrast,
IL-4,
IL-5,
IL-13,
IL-33
maintain
lean
state.
resulting
regulatory
immunomodulatory
pathways
underlying
diseases
have
been
hypothesized
one
mechanisms
increases
risk
severity.
Reduction
weight
diet,
exercise,
or
bariatric
surgery
reduces
activity
improves
lung
function.
International Immunology,
Journal Year:
2024,
Volume and Issue:
36(5), P. 211 - 222
Published: Jan. 16, 2024
Abstract
The
epithelial
barrier
theory
links
the
recent
rise
in
chronic
non-communicable
diseases,
notably
autoimmune
and
allergic
disorders,
to
environmental
agents
disrupting
barrier.
Global
pollution
toxic
agent
exposure
have
worsened
over
six
decades
because
of
uncontrolled
growth,
modernization,
industrialization,
affecting
human
health.
Introducing
new
chemicals
without
any
reasonable
control
their
health
effects
through
these
years
has
led
documented
adverse
effects,
especially
on
skin
mucosal
barriers.
These
substances,
such
as
particulate
matter,
detergents,
surfactants,
food
emulsifiers,
micro-
nano-plastics,
diesel
exhaust,
cigarette
smoke,
ozone,
been
shown
compromise
integrity.
This
disruption
is
linked
opening
tight-junction
barriers,
inflammation,
cell
death,
oxidative
stress,
metabolic
regulation.
Consideration
must
be
given
interplay
underlying
inflammatory
medications,
affected
tissues.
review
article
discusses
detrimental
effect
barrier-damaging
compounds
involves
cellular
molecular
mechanisms.
Frontiers in Immunology,
Journal Year:
2019,
Volume and Issue:
10
Published: Nov. 29, 2019
EEnvironmental
pollutants
and
allergens
induce
oxidative
stress
mitochondrial
dysfunction,
leading
to
key
features
of
allergic
asthma.
Dysregulations
in
autophagy,
mitophagy,
cellular
senescence
have
been
associated
with
environmental
pollutant
allergen-induced
stress,
secretion
multiple
inflammatory
proteins,
subsequently
development
Particularly,
particulate
matter
2.5
(PM2.5)
has
reported
autophagy
the
bronchial
epithelial
cells
through
activation
AMP-activated
protein
kinase
(AMPK),
drive
mitophagy
activating
PTEN-induced
1(PINK1)/Parkin
pathway,
cell
cycle
arrest
senescence.
Intriguingly,
allergens,
including
ovalbumin
(OVA),
alternaria
alternata,
cockroach
allergen,
also
shown
different
signaling
pathways.
Additionally,
dysfunction
can
due
excessive
ROS
production,
which
affects
airway
diseases.
Although
share
similar
properties,
recent
studies
suggest
that
either
accelerate
or
prevent
Thus,
this
review,
we
evaluated
literature
regarding
basic
processes,
senescence,
explored
their
molecular
mechanisms
regulation
initiation
downstream
signaling.
Especially,
highlighted
involvement
pollutant/allergen-induced
major
phenotypic
changes
asthma
such
as
inflammation
remodelling
reviewed
novel
critical
research
areas
for
future
studies.
Ultimately,
understanding
regulatory
may
allow
new
therapeutic
targets
Journal of Clinical Investigation,
Journal Year:
2021,
Volume and Issue:
131(5)
Published: Feb. 28, 2021
IgE
induced
by
type
2
immune
responses
in
atopic
dermatitis
is
implicated
the
progression
of
to
other
allergic
diseases,
including
food
allergies,
rhinitis,
and
asthma.
However,
keratinocyte-derived
signals
that
promote
ensuing
diseases
remain
unclear.
Herein,
a
mouse
model
dermatitis-like
skin
inflammation
epicutaneous
Staphylococcus
aureus
exposure,
keratinocyte
release
IL‑36α
along
with
IL-4
triggered
B
cell
class-switching,
plasma
differentiation,
increased
serum
levels-all
which
were
abrogated
IL-36R-deficient
mice
or
anti-IL‑36R-blocking
antibody-treated
mice.
Moreover,
allergen
sensitization
during
S.
exposure-induced
IL-36
was
required
for
development
allergen-specific
lung
inflammation.
In
translating
these
findings,
elevated
IL‑36
cytokines
human
receptor
antagonist-deficiency
patients
coincided
levels.
Collectively,
keratinocyte-initiated
represent
key
mechanism
potential
therapeutic
target
against
diseases.
Journal of the European Academy of Dermatology and Venereology,
Journal Year:
2022,
Volume and Issue:
36(9), P. 1432 - 1449
Published: May 16, 2022
Atopic
dermatitis
(AD)
is
a
chronic,
heterogenous,
inflammatory
skin
disorder
associated
with
high
skin-related
health
burden,
typically
starting
in
childhood
and
often
persisting
into
adulthood.
AD
characterized
by
wide
range
of
clinical
phenotypes,
reflecting
multiple
underlying
pathophysiological
mechanisms
interactions
between
genetics,
immune
system
dysregulation
environmental
factors.
In
this
review,
we
describe
the
diverse
cellular
molecular
involved
AD,
including
critical
role
T-cell-driven
inflammation,
primarily
via
T
helper
(Th)
2-
Th17-derived
cytokines,
many
which
are
mediated
Janus
kinase
(JAK)
signaling
pathway.
These
local
processes
interact
sensory
neuronal
pathways,
contributing
to
manifestations
itch,
pain
sleep
disturbance.
The
recent
elucidation
pathways
has
allowed
treatment
strategies
evolve
from
broad-acting
systemic
immunosuppressive
therapies
more
targeted
agents,
JAK
inhibitors
cytokine-specific
biologic
agents.
Evidence
development
these
reinforced
expanded
our
understanding
holds
promise
for
individualized
tailored
specific
subtypes.
Contact Dermatitis,
Journal Year:
2021,
Volume and Issue:
85(6), P. 615 - 626
Published: Aug. 22, 2021
Abstract
The
“epithelial
barrier
hypothesis”
proposes
that
the
exposure
to
various
epithelial
barrier–damaging
agents
linked
industrialization
and
urbanization
underlies
increase
in
allergic
diseases.
constitutes
first
line
of
physical,
chemical,
immunological
defense
against
environmental
factors.
Recent
reports
have
shown
industrial
products
disrupt
barriers.
Innate
adaptive
immune
responses
play
an
important
role
damage.
In
addition,
recent
studies
suggest
dysfunction
plays
essential
pathogenesis
atopic
march
by
allergen
sensitization
through
transcutaneous
route.
It
is
evident
external
factors
interact
with
system,
triggering
a
cascade
complex
reactions
damage
barrier.
Epigenetic
microbiome
changes
modulate
integrity
Robust
simple
measurements
skin
at
point‐of‐care
are
significant
value
as
biomarker,
recently
reported
using
electrical
impedance
spectroscopy
directly
measure
defects.
Understanding
its
mechanism
key
developing
novel
strategies
for
prevention
treatment
aim
this
review
summarize
on
pathophysiological
mechanisms
triggered
contribute
dysregulation
function.
Environments,
Journal Year:
2022,
Volume and Issue:
9(7), P. 86 - 86
Published: July 6, 2022
The
world
population
is
ageing,
in
particular
the
developed
world,
with
a
significant
increase
percentage
of
people
above
60
years
old.
They
represent
segment
that
more
vulnerable
to
adverse
environmental
conditions.
Among
them,
indoor
air
quality
one
most
relevant,
as
elders
spend
comparatively
time
indoors
than
younger
generations.
Furthermore,
recent
COVID-19
pandemic
contributed
immensely
raising
awareness
importance
breathing
for
human
health
and
fact
vector
airborne
infections
poisoning.
Hence,
this
work
reviews
state
art
regarding
elderly
centers,
considering
type
pollutants
involved,
their
emission
sources,
effects.
Moreover,
influence
ventilation
on
also
addressed.
Notwithstanding
potential
problems
corresponding
costs
morbidity
effects,
only
few
studies
have
considered
explicitly
its
impacts
health.
More
are,
therefore,
necessary
objectively
identify
what
are
due
how
it
can
be
improved,
either
by
reducing
sources
or
adequate
thermal
comfort
strategies.
Journal of Personalized Medicine,
Journal Year:
2022,
Volume and Issue:
12(1), P. 66 - 66
Published: Jan. 7, 2022
Asthma
is
a
complex
multifactorial
and
heterogeneous
respiratory
disease.
Although
genetics
strong
risk
factor
of
asthma,
external
internal
exposures
their
interactions
with
genetic
factors
also
play
important
roles
in
the
pathophysiology
asthma.
Over
past
decades,
application
high-throughput
omics
approaches
has
emerged
been
applied
to
field
asthma
research
for
screening
biomarkers
such
as
genes,
transcript,
proteins,
metabolites
an
unbiased
fashion.
Leveraging
large-scale
studies
representative
diverse
population-based
data
integrating
clinical
led
better
profiling
risk.
Yet,
date,
no
omic-driven
endotypes
have
translated
into
practice
management
In
this
article,
we
provide
overview
current
status
namely,
genomics,
transcriptomics,
epigenomics,
proteomics,
exposomics,
metabolomics.
The
development
multi-omics
integrations
briefly
discussed.
Biomarker
discovery
following
could
be
challenging
but
useful
disease
phenotyping
endotyping
that
can
translate
advances
care,
ultimately
leading
successful
precision
medicine
approaches.