Germs living on normal Skin and the changes observed in Atopic Dermatitis (Microbiome)

Abbreviations: AD=Atopic Dermatitis

-The Microbiome is in fact microbiota and this terms designates the community of germs (bacteria, viruses and fungi) present since birth
-The amount of the total human microbiome amount to approximately 1.5Kg (1-3% of the body mass)
-Microbiota produce 10 times more cells than the whole body: from this one can wonder who is the guest and who is the host
–Proteins (Gene products) produced by these germs can interfere with the innate and adaptive immune system.
-Microbiota could had a role to play in:

• Inflammatory Bowel Disease (Crohn’s disease)
• Diabetes, Obesity
• Rheumatoid Arthritis
• Colon Cancer
• Allergies
• Neuropsychiatric disease
• “Gut feeling”: when feeling sick and no cause can be found, it could be explained by circumstances in the skin microbiome.

-The types and density of germs vary according to location:

• Sebaceous sites
• Moist sites: (anticubital  and popiteal sites); these are the areas where AD lesions preferentially occur and where the concentration of germs is the highest.
• Dry sites

-The skin microbiome is the most unstable one of the body and is influenced by:

• the environment: this includes: occupation, diabetes, climate, geography. Note: A kiss induces an echange of 80 million germs in 10 seconds !
• the skin barrier (genetics): filaggrin influences the skin micro biome. Influences of this unstable influences by climate geography, diabetes, occupation, hygiene, sex, age and site
• constitutional factors: site, age, sex

-Normal skin has a functional “menage a 3”:

• Toll-like receptors (1) located on keratinocytes (2) enable dendritic cells (3) (part of innate immune immunity) to modulate the adaptive immunity.
• This interplay is a way to maintain skin surface equilibrium.  (Il4 and 14 downregulate the production of natural antimicrobial peptide)
• In AD: there is a lack of adequate response from dendritic cells and Th17 (T helper lymphoctyes).  The dendritic cells are therefore less sensitive due to a downregulation of toll-like receptors. In contrast there is an increased presence of Staphlococcus Aureus bacteria.

-Observations:

• an increased diversity of the skin microbiome compatible with healthy skin. In AD the microbiome is less diverse with the presence of Staphylococcus Aureus (SA). It is not known if this is the cause or the consequence of the flaring.
• Some people automedicate by leaving on antiseptics and it is interesting to see how the reduction of microbiome diversity results on forsenign of AD

To read more about how skin surface properties can influence the skin, click HERE

–With all this science, what therapeutic advice can be given in practice ?

• control inflammation (topicals)
• control xerosis (emollients)
• improve the microbiome: exploration of topical Probiotics. Based on application of live bacterial cultures or bacterial extracts. At the time of publication, nothing published.
• treat earlier rather than later

-Q and A

1. Should people with AD have a pet ?
   If a pet is desired, choose a dog rather than a cat. If a cat its effects by having a dog as a second pet.
2. How does the mite Demodex Folliculorum influence AD ?
   Demodex folliculorum : it is difficult to say whether its effects are positive or negative as this mite has its OWN microbiome

Microbiome and atopic dermatitis. Thomas Bieber (Bonn, Germany). SY01 – Atopic Dermatitis. World Congress of Dermatology 2015 –  Vancouver, Canada