The skin fungus-induced Th1- and Th2-related cytokine, chemokine and prostaglandin E2 production in peripheral blood mononuclear cells from patients with atopic dermatitis and psoriasis vulgaris.
BACKGROUND
It is suggested that skin fungi may be involved in the development of atopic dermatitis (AD) and psoriasis vulgaris (PV).


OBJECTIVE
We studied skin fungus-induced Th1- or Th2-related cytokine, chemokine and prostaglandin E2 (PGE2) secretion in peripheral blood mononuclear cells (PBMC) from patients with AD and PV and normal subjects.


METHODS
PBMC were cultured with the extracts of Malassezia furfur (MF), Candida albicans (CA) and Trichophyton rubrum (TR). The cytokine, chemokine and PGE2 amounts in the supernatants were measured by enzyme-linked immunosorbent assays.


RESULTS
MF induced IL-4 and macrophage-derived chemokine (MDC) secretion in AD patients, while induced IFN-gamma and interferon-inducible protein of 10 kDa (IP-10) secretion in PV patients, however, did not induce either secretion in normal subjects. CA induced IL-4, MDC, IFN-gamma and IP-10 secretion in AD and PV patients and normal subjects. In AD patients, the magnitude of IL-4 and MDC responses to CA was higher than that to MF. Compared with PV patients and normal subjects, the magnitude of IL-4 and MDC responses to CA was higher while that of IFN-gamma and IP-10 responses to CA was lower in AD patients. TR induced moderate IL-4 and MDC secretion only in AD patients. The three fungi induced higher levels of PGE2 secretion in AD patients than in PV patients and normal subjects. Cyclooxygenase-2 inhibitor NS-398 suppressed PGE2 responses to MF, CA and TR, and partially suppressed IL-4 and MDC responses to MF, CA and TR, while enhanced IFN-gamma and IP-10 responses to CA in AD patients, and these effects of NS-398 were reversed by cyclic AMP analogue.


CONCLUSIONS
AD patients manifest Th2-skewed responses to MF, CA and TR, which may be partially attributable to the enhanced PGE2 responses to these fungi. PV patients manifest Th1-skewed responses to MF.
Department of Dermatology, Teikyo University, School of Medicine, Tokyo, Japan.
N
N
Kanda
K
K
Tani
U
U
Enomoto
K
K
Nakai
S
S
Watanabe
D000328:Adult; D000946:Antigens, Fungal / Q000009:adverse effects*; D002176:Candida albicans / Q000276:immunology; D016022:Case-Control Studies; D054422:Chemokine CCL22; D054357:Chemokine CXCL10; D019742:Chemokines, CC / Q000276:immunology; D019743:Chemokines, CXC / Q000276:immunology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003876:Dermatitis, Atopic / Q000276:immunology / Q000382:microbiology*; D003881:Dermatomycoses / Q000276:immunology*; D015232:Dinoprostone / Q000378:metabolism; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007371:Interferon-gamma / Q000276:immunology; D015847:Interleukin-4 / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology; D008290:Malassezia / Q000276:immunology*; D008297:Male; D009578:Nitrobenzenes / Q000494:pharmacology; D011565:Psoriasis / Q000276:immunology / Q000382:microbiology*; D011720:Pyrazoles / Q000494:pharmacology; D013449:Sulfonamides / Q000494:pharmacology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014249:Trichophyton / Q000276:immunology
D000946:Antigens, Fungal; C515482:CCL22 protein, human; D054422:Chemokine CCL22; D054357:Chemokine CXCL10; D019742:Chemokines, CC; D019743:Chemokines, CXC; D016861:Cyclooxygenase Inhibitors; D009578:Nitrobenzenes; D011720:Pyrazoles; C115461:SC 560; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D015847:Interleukin-4; D007371:Interferon-gamma; D015232:Dinoprostone; D007213:Indomethacin