Seborrhoeic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry.
BACKGROUND
The fact that Pityrosporum ovale plays a part in seborrhoeic dermatitis is well established but the mechanism of this relationship has not been established.


OBJECTIVE
To compare the number and type of inflammatory cells and mediators in skin biopsies from normal and lesional skin from the trunk and scalp in patients with seborrhoeic dermatitis, Pityrosporum (Malassezia) folliculitis and in normal skin from healthy controls.


METHODS
The skin biopsies were stained using the labelled Streptavidin-biotin


METHODS
The following markers were studied: CD4, CD8, CD68, HLA-DR, NK1, CD16, C1q, C3c, IgG, CD54 (ICAM-1), interleukin (IL) -1alpha, IL-1beta, IL-2, IL-4, IL-6, IL-10, IL-12, tumour necrosis factor-alpha and interferon-gamma.


RESULTS
HLA-DR+ cells were seen in the highest number, and were higher in lesional skin compared with normal skin from both patients and healthy volunteers. ICAM-1 expression was also increased in lesional skin. C1q and the interleukins showed an increased cellular and intercellular staining in patients compared with healthy controls and the intercellular staining was often more intense in lesions compared with non-lesional skin. Staining was often more intense when Malassezia (Pityrosporum ovale) yeast cells were present.


CONCLUSIONS
An increase in NK1+ and CD16+ cells in combination with complement activation indicates that an irritant non-immunogenic stimulation of the immune system is important. The result with the interleukins showed both an increase in the production of inflammatory interleukins as well as in the regulatory interleukins for both TH1 and TH2 cells. Similarities to the immune response described for Candida albicans infections indicate the role of Malassezia in the skin response in seborrhoeic dermatitis and Pityrosporum folliculitis.
Faergemann
J
J
Department of Dermatology, Sahlgrenska University Hospital, S-413 45 Gothenburg, Sweden. jan.faergemann@derm.gu.se
Bergbrant
I M
IM
Dohsé
M
M
Scott
A
A
Westgate
G
G
D000328:Adult; D003167:Complement Activation; D012628:Dermatitis, Seborrheic / Q000276:immunology* / Q000382:microbiology; D003881:Dermatomycoses / Q000276:immunology*; D005260:Female; D005499:Folliculitis / Q000276:immunology* / Q000382:microbiology; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007124:Immunoenzyme Techniques; D016130:Immunophenotyping; D018836:Inflammation Mediators / Q000378:metabolism*; D007378:Interleukins / Q000378:metabolism; D008290:Malassezia; D008297:Male; D008875:Middle Aged; D012867:Skin / Q000276:immunology
D006684:HLA-DR Antigens; D018836:Inflammation Mediators; D007378:Interleukins