Etiology & Pathophysiology
Emotional
stress
influences
the
course
of
acne.
Cutaneous
neurogenic
factors
including
neuropeptides,
neuropeptide-degrading
enzymes
and
neurotrophic
factors,
are
associated
with
inflammation
in
the
pathogenesis
of
acne.
An
increase
in
the
number
of
mast
cells
around
the
sebaceous
glands
is
also
a
factor.
Substance
P
(SP)-immunoreactive
nerve
fibres
are
close
to
the
sebaceous
glands.
SP,
a
neuropeptide,
stimulates
lipogenesis
of
the
sebaceous
glands,
which
may
be
followed
by
proliferation
of
Propionibacterium
acnes
(a
gram-positive
anaerobic
bacillus
rod).
This
paves
the
way
for
inflammatory
reactions
via
the
mast
cells.
Although
Acne
vulgaris
is
not
life-threatening,
it
is
very
much
a
condition
with
serious
psychological
effects
such
as
morbidity,
decreased
self-esteem,
depression,
and
social
withdrawal.
In
acne
vulgaris
abnormal
keratinisation
,
-
hormonal
function
,
-
bacterial
growth
,
and
i
mmune
hypersensitivity
are
involved.
This
is
common
during
puberty
when
sebaceous
glands
are
particularly
active
in
pilosebaceous
follicles
of
the
head
and
chest.
Over-production
of
sebum
is
stimulated
by
androgens
and
this
increased
production
is
associated
with
plugged
follicle
pores,
which
may
become
inflamed
and
develop
into
inflammatory
acne.
This
inflammatory
acne
may
be
a
direct
response
to
the
follicular inhabitant
Propionibacterium acnes
, which is a member of normal cutaneous flora.
Stress
stimulates
the
corticotropin-releasing
hormone
(CRH)
system.
Receptors
of
corticotropin-releasing
factor
(CRF)
are
present
in
human
skin,
as
are
mast cells. Stress-related crosstalk between mast cells, neurons and keratinocytes plays a significant role in all dermatological pathologies.
CRH
is
capable
to
induce
lipid
synthesis,
steroidogenesis
and
interact
with
testosterone
and
growth
hormone.
An
overly-vigorous
immune
response
to
Propionibacterium
acnes
(P.
acnes)
is
a
fundamental
problem
in
acne
vulgaris.
These
bacteria
secrete
polypeptides,
like
extracellular
enzymes,
such
as
proteases,
hyaluronidases
and
neuroaminidases,
which
can
involve
epithelium
permeabilization
and
inflammatory
infiltration.
P.
acnes
produces
both
chemotactic-
and
pro-inflammatory
cytokine
inducing
factors.
Early-infiltrated
lesions
consist
of
polymorphonuclear
cells.
These
cells
attract
T-helper
cells
of
the
CD4
phenotype,
also
known
as
T4
cells.
Antibodies,
specifically-aimed
at
P.
acnes
antigenic
determinants,
are
IgG
and
IgA
immunoglobulins.
Since
the
Toll
like
receptor
TLR2
plays
a
role
in
the
aetiology
of
acne,
its
stimulation
by
P.
acnes
gives
rise
to
the
production
of
Interleukin-8
(IL-8)-
and
Interleukin-12 (IL-12) pro-inflammatory cytokines.
TARGETS
Propionibacterium acnes bacteria
Mast cells
Corticotropin-releasing factor (CRF)
Cytokines IL-8 and IL-12
Type1 5-α-reductase
5-Lipoxygenase
Tyrosinase
Reactive oxygen species (ROS)
COUNTERACTIONS
Anti-bacterial
Degranulation
Inhibition
Inhibition
Inhibition
Inhibition
Inhibition
Inhibition
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GOD’S HEAVENLY CHALLENGE…
ACNE VULGARIS
1 Corinthians 10:13
“No trial has overtaken you that is not faced by others. And God is faithful: He will not let you be tried beyond
what you are able to bear, but with the trial will also provide a way out so that you may be able to endure it. “
– NET Bible
GOD’S HEAVENLY GARDEN GRACE “WAY OUT”…
Divine molecules locked up within his global garden…molecules such as…
… and many, many, many more