IGE-SENSITIZATION TO CELLULAR AND CULTURE FILTRATES OF FUNGAL EXTRACTS IN PATIENTS WITH ATOPIC-DERMATITIS

Background: Patients with atopic dermatitis may experience exacerbatio ns of eczema triggered by various inflammatory stimuli. One mechanism may be IgE-mediated reactions to dermatophytes since these patients ar e more likely to acquire skin infections with dermatophytes and may be come sensitized. Objective: This study investigates IgE-sensitization to fungi in patients with atopic dermatitis and compares the biologic activity of culture filtrates and cellular fungal extracts. The follow ing allergen extracts were provided as culture filtrates and cellular extracts: Candida albicans, Fusarium moniliforme, and Penicillium nota tun. In addition, Pityrosporum ovale and Trichophyton rubrum cultures were included in the test panel. Methods: Fifteen patients with clinic al findings suggesting dermatophytosis and 11 controls were selected. Each subject was tested by leukocyte histamine release and skin prick test to each fungal extract. The extracts were separated and reduced b y sodium dodecylsulfate polyacrylamide gel electrophoresis and analyze d by IgE-immunoblotting with sera from all study subjects. Results: Fo urteen patients (93%) reacted to one or several fungal extracts by rel easing histamine when challenged in vitro. By immunoblotting experimen ts, patient sera showed binding to a wide range of components in all e xtracts. Patient sera recognized allergenic components shared by cultu re filtrates and cellular extracts but with higher frequent and greate r intensity in culture filtrates. Although culture filtrates generated more frequent and potent IgE-reactions than the cellular extracts, th e difference was not statistically significant. Biologic potency was s imilar when evaluated by skin prick tests and leukocyte histamine rele ase. Conclusion: Patients with atopic dermatitis may develop specific IgE-antibodies to a number of fungi as demonstrated by IgE-immunoblott ing. In selected patients, fungi may trigger an IgE-mediated reaction that may contribute to the exacerbation of eczema. Approximately, one- half of the patients, however, produced IgE-antibodies to fungal (glyc o)proteins without a significant histamine release or skin test respon se possibly because of nonspecific interaction with carbohydrate moiet ies on IgE and poor biologic activity of IgE antibodies directed to cr oss-reactive carbohydrate determinants of fungal glycoproteins. This w arrants caution when interpreting clinical relevance of serologic meas urements of fungal IgE-antibodies.