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Updated: Sep 26, 2026

Infecting Mice with Malassezia spp. to Study the Fungus-Host Interaction
Published on: November 6, 2019
[Malassezia and atopic dermatitis]
Hiroshi Kawaguchi1, Kazuo Akiyama
1Clinical Research Center, National Sagamihara Hospital, Sakuradai 18-1, Sagamihara 228-8522, Japan.
Abstract:
Although many exacerbating factors for atopic dermatitis (AD) have been discussed, we are focusing on fungus antigen as a pathogenesis for this condition. About half of the patients were sensitized by Candida albicans and/or Malassezia furfur (MF) using IgE. Patients with severe eruption tended to have a higher concentration of specific IgE. IgE to purified antigens such as manganese superoxide dismutase (MnSOD), cyclophilin, and Malf2 from MF was also detected, while the pattern of positive IgE was varied among the patients so that the major allergen could not be determined. Skin testing gave a positive reaction to MF after 24 hours as well as an immediate type reaction; this delayed type reaction was AD specific since a small number of patients with bronchial asthma showed a positive response to MF. Peripheral mononuclear cells co-cultured with crude MF antigen in vitro produced IL-5 in some AD patients. This response was correlated with the severity of facial eruption, indicating that Th2 type response to MF might make these eruptions worse. MF was easily detected from various skin regions,but we were not able to explain why fewer colonies were obtained from a region with dermatitis than from a non-dermatitis region. From these results, we speculate there are patients who have IgE and Th2 cells which respond to MF. The exact mechanism, however, is still obscure as to how normal flora such as MF can react and exacerbate AD. Further investigations should be done to learn more about the relationship between AD and MF.
Insights
Fungus like Malassezia furfur (MF) may worsen atopic dermatitis (AD) by triggering IgE and Th2 cell responses. Further research is needed to clarify this complex relationship and its mechanisms.
Area of Science:
- Immunology
- Dermatology
- Microbiology
Background:
- Atopic dermatitis (AD) exacerbation factors are diverse.
- This study investigates the role of fungal antigens in AD pathogenesis.
- Focuses on Candida albicans and Malassezia furfur (MF) as potential triggers.
Purpose of the Study:
- To explore the sensitization to fungal antigens in atopic dermatitis patients.
- To investigate the immunological response to Malassezia furfur (MF) in AD.
- To determine the correlation between fungal sensitization and AD severity.
Main Methods:
- Immuno-assays to detect specific IgE against fungal antigens.
- Skin testing to assess immediate and delayed hypersensitivity reactions to MF.
- In vitro co-culture of peripheral mononuclear cells with MF antigen to measure IL-5 production.
Main Results:
- Approximately 50% of AD patients showed IgE sensitization to Candida albicans and/or MF.
- Higher specific IgE concentrations correlated with severe AD eruptions.
- A specific delayed-type skin reaction to MF was observed in AD patients, suggesting a Th2-mediated immune response implicated in exacerbating facial eruptions.
Conclusions:
- Patients with atopic dermatitis may exhibit IgE and Th2 cell responses to Malassezia furfur.
- The precise mechanisms by which MF exacerbates AD remain unclear.
- Further investigation is warranted to elucidate the relationship between MF and AD.
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