Malassezia and atopic dermatitis

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.