Several microbiotas are involved in atopic dermatitis

Vignette

Atopic dermatitis is the most common inflammatory disease of the skin. It is characterized by an excessive immune reaction and modification of the endogenous flora, and affects 20% of children and 10% of adults. Current research focuses on the relationships between the microbiota and the mechanisms which trigger the disease. The effects of a dysbiosis seem to be decisive, whether the epidermis, the nose or the intestinal mucosa are affected.

 

The role of the microbiota in the development of chronic skin disorders is becoming clear, as shown by two studies on atopic dermatitis (AD). The first, a Danish study, enrolled around 100 adults, including 56 with AD. The objective was to study the link between disease severity, microbial composition and host genetics. More specifically, the researchers analyzed the skin and nasal microbiota as well as mutations in the gene encoding filaggrin (FLG), a major risk factor in AD.

Overly homogeneous flora, increased severity

The skin microbiota of atopic patients was different from that of control patients, including those who did not present with visible lesions. Epidermal remodeling (change in pH, lipid profile, and transepidermal water loss, etc.) could then occur, even without apparent clinical manifestations. The diversity of the microbiota is diminished, which seems to be partially corrected by topical corticosteroids. In patients with lesions, this diversity was even lower, and disease severity was all the greater where there was little diversity of microbiota and overabundance of Staphylococcus aureus. Genetic differences appeared exclusively in patients without lesions, in whom a larger number of mutations of the FLG gene was correlated with a higher proportion of Staphylococcus caprae. This result was not observed in patients with lesions, perhaps because of the dominance of S. aureus, which is thought to skew analyses. It should also be noted that the nasal microbiota of atopic patients was less diverse than that of control patients, suggesting a migration of the skin microbiota to the nasal bacterial community.

Infantile AD and feeding

A team from South Korea explored the role of the intestinal microbiota in AD in 129 six-month-old babies, 63 of whom had the disease, as a function of the type of milk consumed (maternal or mixed). Analysis of the bacterial composition by 16S rRNA sequencing did not reveal any significant difference between healthy and atopic infants (stratification of the atopic infants was based only on the feeding method). Conversely, the functional metagenomics approach revealed that the genes associated with immunity were less abundant and different in atopic babies depending on the feeding method used. In children with AD who had received mixed feeding, these differences were associated with a reduction in mucin-degrading bacteria, such as Akkermansia muciniphila and Ruminococcus gnavus, which are thought to supply nutrients to colonizing bacteria when the microbiota is becoming established. In infants with AD, decreased levels of these bacteria could lead to a delay in bacterial colonization and impaired maturation of the immune system. It thus seems that skin health is also linked to that of our intestines.

 

Sources: 

Clausen ML et al. Association of Disease Severity With Skin Microbiome and Filaggrin Gene Mutations in Adult Atopic Dermatitis. JAMA Dermatol 2018 Jan

Lee MJ et al. Perturbations of the gut microbiome genes in infants with atopic dermatitis according to feeding type. J Allergy Clin Immunol 2018; S0091-6749(18)30033-2