Arachidonic acid released from epithelial cells by Malassezia furfur phospholipase A₂: a potential pathophysiologic mechanism

Abstract

Malassezia furfur is a lipophilic yeast that has been related to inflammatory skin conditions such as seborrhoeic dermatitis and psoriasis. We have previously reported that this yeast secretes enzymes capable of metabolizing complex lipids. This lipolytic system is critical for M. furfur growth, since the yeast has a strict dependence on an exogenous source of fatty acids. In the present study we show that M. furfur can grow in cultures supplemented with either Hep-2 cell membranes or erythrocytes as the sole source of lipids. M. furfur secretes enzymes having phospholipase A₂ activity, based upon the lysis of erythrocytes being inhibited by pretreatment with p-bromophenacyl-bromide. This enzyme liberates arachidonic acid from Hep-2 cells, as confirmed by High Performance Liquid Chromatography and High Performance Thin Layer Chromatography analysis. Arachidonic acid metabolites are well-known mediators of skin inflammation. Biopsies taken after topical inoculations of mice with M. furfur culture supernatant show evidence of an inflammatory response. As a result of our findings, we established that M. furfur can trigger an inflammatory response per se by releasing metabolic products.

Key Words:

• Eicosanoids
• skin inflammation
• lipase
• yeast