Editor: Artur Ulmer
Cytokine secretion profile of human keratinocytes exposed to Malassezia yeasts
Article first published online: 27 OCT 2006
FEMS Immunology & Medical Microbiology
Volume 48, Issue 3, pages 400–409, December 2006
How to Cite
Ishibashi, Y., Sugita, T. and Nishikawa, A. (2006), Cytokine secretion profile of human keratinocytes exposed to Malassezia yeasts. FEMS Immunology & Medical Microbiology, 48: 400–409. doi: 10.1111/j.1574-695X.2006.00163.x
- Issue published online: 27 OCT 2006
- Article first published online: 27 OCT 2006
- Received 20 April 2006; revised 7 August 2006; accepted 4 September 2006.First published online 27 October 2006.
- atopic dermatitis;
The lipophilic yeast Malassezia is an exacerbating factor in atopic dermatitis (AD). Among organisms of the Malassezia species, Malassezia globosa and Malassezia restricta are particularly dominant on the skin of AD patients. However, the precise role of Malassezia yeasts in the pathophysiology of AD remains uncertain. Keratinocytes play a critical role in cutaneous inflammatory and immune responses by secreting cytokines. In this study, we attempted to determine the cytokine secretion profiles of human keratinocytes that were exposed to Malassezia yeasts. The human keratinocyte cell line PHK16-0b was cocultivated with M. globosa or M. restricta for 24 h, and the resulting cytokine secretion profile was analysed using a cytokine antibody array. The keratinocytes responded to the two Malassezia species with different Th2-type cytokine profiles, i.e. M. globosa induced IL-5, IL-10 and IL-13 secretion from the keratinocytes, whereas M. restricta induced IL-4 secretion. Similar results were obtained with primary normal human epidermal keratinocytes. cDNA microarray analysis confirmed that IL-5, IL-10, and IL-13 mRNAs were induced only by M. globosa, while IL-4 mRNA expression was induced only by M. restricta. These findings suggest that M. globosa and M. restricta play a synergistic role in triggering or exacerbating AD by stimulating the Th2 immune response.