the growth of both S. aureus and S. epidermidis. This suggests that topical treatments promoting P. acnes growth may reduce S. aureus growth, which could help in AD management.9
Propionibacterium is the primary genus on the forehead and cheeks of healthy females. As sebum on the cheek increases, so the prevalence of Propionibacterium increases while the microbiome diversity decreases.11 The excess of sebum on the face compared with the body can therefore lead to increased Propionibacterium levels, ultimately inhibiting S. aureus, and limiting inflammation when compared with those with AD. Clinical studies support using topical commensal organisms, specifically Staphylococcus hominis and Roseomonas mucosa, to treat AD.12
The topography of skin influences its microflora balance.13 Eccrine sweat glands are more highly concentrated in the forehead and cheeks than in the trunk.14 Sebaceous glands, which are highly concentrated on the face, chest, and back, favor the growth of lipophilic organisms, such as Malassezia species. Sweat, a known aggravator of AD, also increases Malassezia growth.15 Malassezia plays a role in the pathogenesis of AD through the production of proinflammatory cytokines and activation of auto-reactive T cells.16-17 Furthermore, adults with AD are often sensitized to yeast, as evidenced by specific IgE antibodies to Malassezia species.18 Specifically, the fungal protein MGL_1304 derived from Malassezia globosa can induce basophils to release histamine, and IgE antibodies against this antigen are in the sera of patients with AD, contributing to a type I hypersensitivity reaction.19
