Abstract
Purpose: To establish atopic dermatitis (AD) mouse models infected with Malassezia globosa and study its effects and potential mechanisms. Methods: Twenty - four male BALB/c mice were randomly allocated into four groups: control, AD, M (normal mice treated with olive oil fungus suspension), and AD + M (AD mice treated with the same suspension). DNFB was used to induce the AD model. The M and AD + M groups were treated with Malassezia suspension. Body weight, scratching behavior, and skin lesion scores of mice were recorded. Skin tissues underwent HE and PAS staining, viable fungal flora counting, and Th1/Th2 cytokine detection via flow cytometry. Results: The AD mouse models infected with Malassezia globosa were successfully set up. The AD + M group scratched more often. On days 8, 12, and 16, the AD group's skin lesion scores were (9.00±0.89), (10.17±0.87), (9.17±0.75), while those of the AD + M group were (11.00±0.82), (10.83±0.75), (10.83±0.75) (P<0.05). The AD + M group had more Malassezia colonization (P<0.001). The M group displayed a Th1 response. The AD + M group enhanced Th1 response and increased Th2 cytokines like IL - 4 and IL - 10 (P<0.05). The control group had normal skin with minimal scratching and low fungal counts. Conclusion: Malassezia causes inflammation in normal and AD - like skin, with worse inflammation when the skin barrier is damaged. Targeting Malassezia might alleviate AD inflammation, offering new AD treatment directions.