Abstract Number: 12

Targeting the human skin microbiome in patients withatopic dermatitis

T.A. Luger

Meeting: 2015 Dermcoll

Atopic dermatitis (AD) is a multigenic chronically relapsing
inflammatory skin disease characterized by eczema and
pruritus. The prevalence of atopic dermatitis (AD) in developed
countries is increasing and currently is ranging from
20% to 25% in children and 2–3% in adults. Recent progress
has been achieved in our understanding about the complex
mechanisms underlying the pathophysiology of atopic dermatitis,
involving an impaired epidermal barrier function,
an abnormal function of both innate as well as adaptive
immune responses and an altered microbiome of the skin.
The human body in particular epithelia, which represent the
barrier to the environment are colonized by a variety of
microorganisms and there is a well-established symbiotic
relationship between host and microbes. The term microbiome
refers to the totality of microorganisms, their
genomes and interactions in a defined environment and is
considered as being an important part of the human metabolic
system. The human body contains 10 times more bacterial
cells than human cells. The human microbiome
consists of about 5–10,000 species and the total of bacteria in
the human organism, is 1–3% of body weight. In the past
studies on the microbiome of the gastrointestinal tract provided
evidence of a relation between the microbiome and
obesity.Initial investigations of the skin microbiome show an
enormous inter-and intra-individual diversity. Thus
actinobacteria are predominant in seborrheic areas of the
skin, while proteobacteria mainly occur in dry skin areas
and firmicutes mostly are located in moist areas. The composition
of the skin microbiome is influenced by many different
factors such as environment, age, gender, metabolic-,
and inflammatory diseases.
In patients with atopic dermatitis, a marked change in the
skin microbiome diversity has been shown as a function of
the disease severity. Thus, the diversity of the microbiome
decreases during disease exacerbation in favor of colonization
with pathogenic microbes such as staphylococcus
aureus. Interestingly, the changes in the skin microbiome
can already be observed before disease exacerbation
occurs. Upon successful topical or systemic treatment an
increase of the diversity associated with a decrease of S.
aureus has been observed. Resident bacteria of the skin
such as S. epidermidis by releasing antimicrobial peptides
as well via stimulating the skin immune system are able to
control the colonization with pathogenic microbes such as
S. aureus.
In the future, the exploration of the skin microbiome will
enable entirely new approaches for the treatment of infectious
and inflammatory skin diseases.