title: Pityrosporum and Candida specific and non-specific humoral, cellular and cytokine responses in atopic dermatitis patients.
abstract: BACKGROUND
  Recent cytokine (RT-PCR, ELISA) analyses of inflammation in atopic dermatitis (AD) have suggested a role for IL-4, IL-5 and IFNgamma. Pityrosporum ovale and Candida albicans are important allergens in some patients with AD of the seborrhoic head, neck and shoulder region. In AD patients, the saprophytic yeasts induce IgE responses while they usually induce TH1 type responses. The cytokine responses induced by yeasts in AD are sparsely investigated.
  
  
  OBJECTIVE
  To characterize the P. ovale- and C. albicans-specific and non-specific humoral, lymphoproliferative and cytokine (IL-2, 4, 5 and IFNgamma) responses in AD.
  
  
  METHODS
  Fifteen AD patients and seven healthy controls (HC) were included. Ficoll-isolated PBMC were stimulated by PHA and laboratory-generated extracts of P. ovale and C. albicans. Lymphocyte proliferation was measured by 3H-thymidine incorporation and cytokine production by sandwich-ELISAs. The antigen-specific IgG and IgE antibodies were analysed by ELISA and nitrocellulose RAST.
  
  
  RESULTS
  Pityrosporum ovale- and C. albicans-specific IgE (both P < 0.001) and P. ovale-induced PBMC proliferation (P < 0.02) were elevated in AD. In general, the IL-4/IFNgamma ratio induced by P. ovale was higher than that induced by C. albicans (P < 0.01). The PHA-induced IL-2 (P < 0.05) and IL-4 responses (P < 0.005), and the C. albicans-induced IL-5 response (P < 0.02) and IFNgamma response (P < 0.01), were elevated in AD. A network of correlations was seen between serum total and the yeast-specific IgE, P. ovale-specific lymphoproliferation, PHA-induced IL-2, IL-4 and IL-5, and C. albicans-induced IL-5.
  
  
  CONCLUSIONS
  The cytokine profiles found in this study support the role of TH0 or TH1 cells by the side of TH2 cells in the pathogenesis of atopic dermatitis. Pityrosporum ovale appears to be associated more with IL-4 responses and C. albicans with IFNgamma responses.
authors.affiliation: Department of Pulmonary Diseases and Clinical Allergology, University of Turku, Finland.
authors.forename: J
authors.initials: J
authors.lastname: Savolainen
authors.forename: P
authors.initials: P
authors.lastname: Lintu
authors.forename: J
authors.initials: J
authors.lastname: Kosonen
authors.forename: O
authors.initials: O
authors.lastname: Kortekangas-Savolainen
authors.forename: M
authors.initials: M
authors.lastname: Viander
authors.forename: J
authors.initials: J
authors.lastname: Pène
authors.forename: K
authors.initials: K
authors.lastname: Kalimo
authors.forename: E O
authors.initials: EO
authors.lastname: Terho
authors.forename: J
authors.initials: J
authors.lastname: Bousquet
mesh_terms: D000328:Adult; D002176:Candida albicans / Q000276:immunology*; D016207:Cytokines / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D008213:Lymphocyte Activation; D008290:Malassezia / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D016207:Cytokines; D007074:Immunoglobulin G; D007073:Immunoglobulin E