Seborrheic dermatitis (SD) is a chronic inflammatory skin disease that causes flakes and erythema on the scalp, eyebrows, nasolabial folds, glabella, and ears. Although it is a common skin disease, its cause is still unclear¹. Previous studies have reported on the associations between immune response and inflammation, microorganisms, abnormal skin lipids, epidermal hyperkeratosis, and neurotransmitter abnormalities. Climate, medications, malnutrition, and genetic factors may also cause SD¹.

SD pathogenesis due to Malassezia, a fungi, and Cuti- bacterium, a bacteria, have been well studied. Several studies have reported that Malassezia furfur weakens the skin barrier function by producing indoles, which are ligands for aryl hydrocarbon receptors, or using oleic and arachidonic acids generated as sebum metabolites². Cutibacterium acnes and Malassezia have lipolytic ability, converting triglycerides into free fatty acids³. Recently, with the development of the micro- biome concept in all fields of dermatology, SD research has expanded to investigate the involvement of mycobiome/ microbiome.

Several studies have confirmed the α- and β-mycobiome diversity in patients with SD. The patient's Shannon index of α diversity has been reported to decrease as well as increase^4,5. Several reports have stated that no difference exists between the lesion and nonlesion areas and according to the body parts^4,6. Another study reported a decrease in the Chao and Simpson indexes⁷.

Regarding β diversity, study results indicating that it is possible to distinguish between the patient and healthy individual as well as those indicating that they cannot be distinguished exist. Further, results regarding the lesion and nonlesion areas are heterogenous^4,7-10. A previous report stated the absence of any difference in diversity according to disease severity10 (Table 1).

Among the fungi constituting the mycobiome, the most well-known is Malassezia. Additionally, it has been reported that fungi, such as Mycosphaerella, Candida, Filobasidium, Aspergillus, Ganoderma, Exidia, Pilatoporus, and Engyodontium, vary in SD. Currently, heterogeneous results indicate the increase or decrease of each species, but the increase in Malassezia, especially M. restricta, and the decrease in M. golbossa, reveal similar results^4-14.

The α-diversity of the SD microbiome showed inconsistent results. Thus, among the outcomes obtained, the relatively consistent one states that no difference between the lesion and nonlesion areas exist^7-9. Regarding the β-diversity, the main opinion is that the sample distance is higher in healthy individuals^4,5,7-9,15 (Table 1). The members of the microbiome include Staphylococcus, Cutibacterium, Streptococcus, Pseudomonas, Actinobacteria, and Firmicutes. It is considered that Staphylococcus and Streptococcus increase while Cutibacterium and Pseudomonas decrease^4-9,12,13,15.

Differences between study results arise due to differences between individuals. Moreover, factors such as residence and race of the population, sampling method, and sequencing techniques differ among studies. Sequencing results also vary depending on the target gene, and there are various methods for sequencing, such as cloning and Sanger sequencing, quantitative polymerase chain reaction, amplicon sequencing, and whole metagenome sequencing; however, currently no standardized sampling or experimental method exists. Therefore, the results are bound to be affected².

For clinically meaningful microbiome changes, it should be confirmed that changes are significantly related to clinical symptoms. However, research is limited on this topic. According to a study by Saxena et al.⁵, M. globosa, known to decrease mainly in SD, showed a negative correlation with total dandruff and itching and a positive correlation with total Malassezia. Also, a decrease in Pseudomonas and an increase in Staphylococcus were positively correlated with dandruff and itch⁵. A positive correlation of Staphylococcus and Cutibacterium with TEWL and water content indicates their potential role in skin barrier function¹². Moreover, researchers have analyzed the functional pathways of the mycobiome/microbiome. The mycobiome are enriched in pathways involved in cell-host adhesion in the dandruff. Contrastingly, the microbiome was enriched in pathways related to the synthesis and metabolism of amino acids, biotin, and other B-vitamins, which have been reported to be essential for hair growth⁵.

For the application of microbiome research in actual clinical practice, it is necessary to check whether dysbiosis improves after treatment and whether this improvement leads to symptom progression, besides examining the relationship between microorganisms and clinical symptoms. However, there is limited research on this field. Leong et al.¹⁶ confirmed the changes in M. restricta and M. globosa in 35 healthy sub- jects before and after using antifungal zinc pyrithione shampoo. On the one hand, M. restricta temporarily decreased after shampooing, but the variation among individuals was large. However, it soon returned to the original state, thus failing to maintain a meaningful change. On the other hand, M. globosa was unaffected by the use of zinc pyrithione sham- poo¹⁶. The following results confirmed the changes in patients with SD using selenium-disulfide shampoo. The participants used 2% ketoconazole shampoo for 1 month. The outcomes showed beneficial results, such as the reduction of dandruff and erythema, restoration of Malassezia diversity, reduction of total Malassezia count, and reduction of Staphylococcus. The participants were classified into two groups. The first group maintained treatment using 1% SeS2-based shampoo, and the other group used a vehicle. It was confirmed that the significant response after using ketoconazole shampoo was well maintained in the group using the selenium shampoo¹⁷.

Rather than regulating existing microbes, some treatments involve supplementation with beneficial microorganisms. Hence, strains known to be helpful against atopic dermatitis in patients with SD can be used, as patients with SD also suffer from barrier damage and skin immune abnormalities, such as atopic dermatitis¹⁸. Vitreoscilla filiformis is a gram-negative bacterium that stimulates regulatory T cells and does not affect the survival of microorganisms constituting the microbiome¹⁹. It has been reported that when applied to patients with atopic dermatitis, it helps to moisturize the skin²⁰. Therefore, when vitreoscilla biomass was applied to SD patients, symptom improvement, such as itching, was observed²¹. The application of the Lactobacillus biomass (Lactobacillus sporogene or Lactobacillus rhamnosus) also appeared to be beneficial in the improvement of both psor- iasis and SD^22,23. Furthermore, another study investigated the reaction after oral ingestion rather than microbial application. SD symptoms, such as dandruff, improved when Lactobacillus paracasei NCC 2461 ST11 was taken once daily²⁴.

In conclusion, SD mycobiome/microbiome diversity can be considered controversial, and presently, this research has relatively decreased. It is possible that the difference between the lesion and nonlesion areas is not significant, and there is a change in species and quantity. Malassezia (esp., restricta), Staphylococcus, and Streptococcus increased in abundance, whereas M. globosa, Cutibacterium, and Pseudomonas de- creased. There are possible correlations between SD symptoms and changes in the microbiome and its metabolic pathways.