Dysbiosis of skin mycobiome in atopic dermatitis

Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease with an increasing prevalence worldwide. The aetiology and pathogenesis of AD have not been fully elucidated. Previous studies have suggested the role of fungi as a triggering factor in the development AD. Here we conducted a systematic review to investigate the skin mycobiome profiles in AD and to address whether there is an association between fungal dysbiosis and AD. We searched Medline/PubMed, Embase and Web of Science for research studies published in English between January 1st, 2010 and April 21st, 2021. A total of 11 human studies and 3 animal studies were included in this analysis. Fungal dysbiosis was observed in AD lesions with a depleted amount of Malassezia and a higher abundance of filamentous fungi. A positive correlation between Candida and Staphylococcus was also demonstrated in AD. We supposed that specific species of Malassezia spp. and Candida spp. may play a role in the pathogenesis of AD by interacting with the pathogenic bacteria. Topical application of emollients could improve the skin barrier function and restore the skin fungal flora by increasing the amount of Malassezia. Further studies focusing on the complex interplay between specific skin fungi and the host can provide better insight into the role of microorganisms in the pathogenesis of AD.

Automated summary

Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease with increasing prevalence worldwide. The etiology and pathogenesis of AD are not fully understood, but previous studies have suggested a potential role of fungi as a triggering factor in its development. Fungal dysbiosis, characterized by decreased Malassezia and increased filamentous fungi, is observed in AD lesions, along with a positive correlation between Candida and Staphylococcus. Further research focusing on the interaction between specific skin fungi and the host can provide better insights into the role of microorganisms in AD pathogenesis.