Trichophyton tonsurans-induced kerion celsi with decreased defensin expression and paradoxically increased interleukin-17A production

J Dermatol. 2019 Sep;46(9):794-797. doi: 10.1111/1346-8138.15008. Epub 2019 Jul 11.

Abstract

We report a case of kerion celsi due to Trichophyton tonsurans. An 18-year-old male student judo practitioner had alopecic patches, black dots and subcutaneous abscesses on the right temporal region. The damaged hair represented endothrix infection with T. tonsurans, as assessed by mycological examinations. He was treated with oral itraconazole without any therapeutic effect, followed by terbinafine with good effect. A skin biopsy showed neutrophil, lymphocyte and histiocyte infiltration into the dermis and subcutaneous tissue with abscesses around a number of dilated hair follicles. Immunostaining showed that the expression level of human β-defensin 2 (HBD-2) was decreased in the epidermis of the alopecic and adjacent skin. Because interleukin (IL)-17A generally induces HBD-2 production by epidermal keratinocytes, we also immunohistochemically investigated IL-17A expression. Unexpectedly, many IL-17A-bearing cells were found around destructed hair follicles, indicating that IL-17A expression was not attenuated, but rather increased in the skin lesion. Our case suggests that IL-17A-upregulated antimicrobial peptide expression is disordered in kerion celsi, and severe inflammation with IL-17A may cause tissue damage and resultant scar.

Keywords: Trichophyton tonsurans; defensin; dermatophytosis; interleukin-17; kerion celsi.

Publication types

  • Case Reports

MeSH terms

  • Adolescent
  • Biopsy
  • Hair Follicle / immunology
  • Hair Follicle / metabolism
  • Hair Follicle / pathology
  • Humans
  • Interleukin-17 / immunology
  • Interleukin-17 / metabolism*
  • Male
  • Tinea Capitis / immunology*
  • Tinea Capitis / microbiology
  • Tinea Capitis / pathology
  • Trichophyton / immunology*
  • Trichophyton / isolation & purification
  • beta-Defensins / immunology
  • beta-Defensins / metabolism*

Substances

  • DEFB4A protein, human
  • IL17A protein, human
  • Interleukin-17
  • beta-Defensins