The skin of patients with atopic dermatitis (AD) is in a state of dysbiosis, having a microbiome of reduced diversity dominated by exacerbators such as Staphylococcus aureus and by fungal taxa such as Malassezia. As the symptoms of AD improve, microbial diversity increases and the level of colonization by exacerbators decreases. The level of skin colonization is correlated with scores on AD evaluation indices, thus the goal of AD treatment is to improve dysbiosis. Although Malassezia species exacerbate AD, they also secrete proteases that inhibit the formation of biofilm by Staphylococcus aureus at non-lesional sites. Therefore, species in this genus may be either beneficial or harmful depending on the host environment. Androgenetic alopecia (AGA) develops when the growth phase of the hair cycle shortens, leading to an increase in the proportion of resting hair follicles. The scalp sebum of individuals with AGA has a higher triglyceride content than those without AGA, leading to greater colonization by Malassezia, which use triglycerides as nutrients. Furthermore, the scalp of AGA individuals (?) is in a state of dysbiosis, and Cutibacterium is replaced by Corynebacterium. This can lead to lipophilic bacterium-induced inflammation, which contributes to the progression of hair loss. This review focuses on two aspects of dermatitis linked to dysbiosis. First, we assess the changes in skin microbiome and cross-domain (bacteria versus fungi) microbial interactions in AD; then we consider the mechanism by which an altered scalp-sebum composition leads to the development of AGA.
Takashi Sugita (2025) studied this question.