News
Article
Author(s):
The study identified 2 fungal profiles in AD patients, with 1 subgroup exhibiting distinct fungal dysbiosis.
Recent studies suggest that dysbiosis of the skin mycobiome, particularly shifts in fungal populations, may contribute to atopic dermatitis (AD) pathogenesis. These findings, from a case-control study comparing the skin mycobiome of those with AD and healthy volunteers (HV), highlight key fungal species and their potential role in AD exacerbation.1
“In this work, conventional identification methods produced a higher culture-positive rate in AD patients than in HV. Moreover, culture-based phenotypic and PCR-sequencing methods used for species identification gave concordant results for 68.6% of the isolates. Such discrepancies only confirm the superiority of molecular methods over conventional, culture-based mycological diagnostics,” researchers behind the study wrote.
Introduction
AD affects up to 20.1% of children and 4.9% of adults worldwide. The condition is characterized by pruritic, eczematous lesions and is frequently associated with increased skin colonization by microbes, including fungi.2,3 The skin mycobiome, composed of diverse fungal species, plays a critical role in maintaining cutaneous homeostasis. Understanding alterations in fungal populations in AD may provide insights into disease mechanisms and potential therapeutic interventions.
Methods
A comparative analysis of the skin mycobiome was conducted on 50 patients with AD and 50 HV. The study employed both culture-dependent methods, including phenotypic tests and PCR sequencing of the internal transcribed spacer (ITS) regions, and culture-independent metataxonomic sequencing. Samples were collected from the antecubital crease, neck, and popliteal fossa for analysis.
Results
The study revealed significant differences in the skin mycobiome between patients with AD and HV. Culture-based methods identified a higher prevalence of fungi in patients with AD (74%) compared to HV (28%). Dominant fungal species in those with AD included Rhodotorula spp., Candida spp., Malassezia spp., and Naganishia albida.
Metataxonomic analysis classified patients with AD into 2 subgroups: ‘control-like’ AD (66%) with fungal profiles similar to HV and ‘AD-specific’ (34%) with distinct fungal compositions. The ‘AD-specific’ subgroup exhibited increased abundance of Cladosporium, Malassezia, Candida, Diplodia, Saccharomyces, Penicillium, and Aspergillus. Notably, researchers found exposure to air-conditioning was significantly associated with the ‘AD-specific’ mycobiome composition (p = 0.030).
Discussion
Findings suggest that fungal dysbiosis, particularly overrepresentation of Malassezia and Candida species, may play a role in AD pathogenesis. Malassezia spp. produce lipases and phospholipases, which can disrupt the epidermal barrier and trigger inflammatory responses. Sensitization to Malassezia has been linked to increased AD severity. Similarly, Candida spp. are known to induce hypersensitivity reactions and may contribute to skin inflammation in AD.
The presence of environmental moulds such as Cladosporium, Penicillium, and Aspergillus in those with AD suggests potential external influences on mycobiome composition. Anthropogenic factors, including air-conditioning, may contribute to these shifts, warranting further investigation into environmental triggers of fungal dysbiosis in AD.
Limitations and Future Directions
While this study provides valuable insights, limitations include the single-center design and the absence of fungal sensitization assessments. The study stated future research should explore the functional role of identified fungal species in AD, including their interaction with bacterial microbiota and host immune responses. Additionally, longitudinal studies assessing the impact of antifungal interventions on AD severity are warranted.
Conclusion
This study highlights significant alterations in the skin mycobiome of AD patients, underscoring the potential role of fungal dysbiosis in disease progression. The findings suggest that fungal species, particularly Malassezia and Candida, may contribute to inflammation and barrier dysfunction in AD. Researchers stated considering environmental factors in future therapeutic strategies may improve patient outcomes.
Want to hear more pearls and expert insights on AD? Join us at the annual Revolutionizing Atopic Dermatitis Conference this June in Nashville, TN.
References