Inhibition of dermatophytes by the antimicrobial peptides human β-defensin-2, ribonuclease 7 and psoriasin

Abstract

Previous studies have described some antibacterial effects of antimicrobial peptides (AMPs) expressed in human skin, but little is known about their possible activity against dermatophytes. Therefore we have tested the effects of human β-defensin 2 (hBD-2), ribonuclease 7 (RNase 7) and psoriasin on the in vitro growth of four dermatophyte species. Germinating conidia of Trichophyton rubrum, T. mentagrophytes, Microsporum canis and Epidermophyton floccosum were exposed in vitro to hBD-2, RNase 7, psoriasin and fluconazole. Subsequent fungal growth was measured photometrically over 168 hours. All AMPs significantly inhibited fungal growth, with the degree of inhibition dependent on the dermatophyte species and the specific AMP. E. floccosum was found to be the most susceptible species in that it was markedly suppressed by all AMPs, whereas M. canis was inhibited only by psoriasin. Overall, psoriasin was the most effective AMP and had even stronger inhibitory effects on some dermatophytes than fluconazole. Our findings show that AMPs expressed in human skin can, in principal, inhibit the growth of dermatophytes in vitro. Therefore the question whether AMPs are relevant for human protection against tineas is justified and should be addressed by investigating their role in vivo.

Low DEFB4 Copy Number and High Systemic hBD-2 and IL-22 Levels Are Associated with Dermatophytosis

“…One interpretation of these results is that IL-22 has a protective role during T. rubrum infection, such that the level of the antimicrobial hBD-2 is upregulated in patients who have low DEFB4 CN and in whom the hBD-2 level is insufficient for an immune response against T. rubrum, which increases their susceptibility to infection. This is supported by a study showing that hBD-2 inhibits T. rubrum growth in vitro (Fritz et al, 2012). Consequently, T. rubrum may induce IL-22 production either directly or indirectly by stimulating other factors known to enhance IL-22, such as tumor necrosis factora and IL-1b (Sonnenberg et al, 2010), leading to the upregulation of DEFB4 gene expression and increased production of hBD-2.…”

Infection of Keratinocytes with Trichophytum rubrum Induces Epidermal Growth Factor-Dependent RNase 7 and Human Beta-Defensin-3 Expression

“…The strains were identified by established morphologic and physiologic criteria [9]. Microconidia were prepared as recently described [6].…”

“…Although the role of AMP to control the growth of bacteria on the skin surface and to protect the skin from infection is widely recognized, the role of AMP in tinea is less explored. Recently, it has been reported that AMP are induced in the lesional epidermis of tinea patients [5] and that the skin-derived AMP psoriasin, hBD-2 and RNase 7 are able to inhibit the growth of dermatophytes in vitro [6]. Thus, there is increasing evidence that AMP may also play an important role in the innate cutaneous defense against dermatophytes.…”

Majocchi’s Granuloma (Dermatophytic Granuloma): Updated Therapeutic Options

“…Humoral-mediated immunity is also involved in fungal infections and mediates the protection against many fungi (Candida spp., T. rubrum) [42], increasing epidermal proliferation and facilitating dermatophyte elimination; however, the exact role of this immunity is uncertain [43][44][45]. It is clear that some parts of the immune system contribute more than others, but they are all important for the overall protection [46].…”