Mycostatic effect of recombinant dermcidin against Trichophyton rubrum and reduced dermcidin expression in the sweat of tinea pedis patients.

Trichophytosis, a common dermatophytosis, affects nearly 20-25% of the world's population. However, little is known about mechanisms for preventing colonization of Trichophyton on the skin. Dermcidin, an antimicrobial peptide that provides innate immunity to the skin and is constitutively secreted even in the absence of inflammatory stimulation, was studied to elucidate its antimycotic activity against Trichophyton. Recombinant dermcidin was determined to have antimycotic activity against Trichophyton rubrum, as evaluated by colony-forming unit (CFU) assays. The killing rate of dermcidin was 40.5% and 93.4% at 50 μg/mL (the average dermcidin concentration in healthy subjects) and 270 μg/mL, respectively. An effect of dermcidin treatment was found to be a reduction of the metabolic activity of Trichophyton as determined by nicotinamide adenine dinucleotide assay. Further, dermcidin concentrations in sweat of tinea pedis patients were found to be lower than those of healthy subjects. These findings suggest a mycostatic role for dermcidin, at normal sweat concentrations. Accordingly, we suspect that dermcidin, at normal sweat concentrations, inhibits growth of Trichophyton, where Trichophyton is subsequently eliminated in conjunction with epidermis turnover. Dermcidin, therefore, appears to play a role in the skin protection mechanism that prevents colonization of tinea pedis.