Cytokine secretion profiles of human keratinocytes during Trichophyton tonsurans and Arthroderma benhamiae infections.
Dermatophytes cause intractable superficial infections in humans. Arthroderma benhamiae, a zoophilic dermatophyte, triggers severe inflammatory responses in humans, while Trichophyton tonsurans, an anthropophilic dermatophyte, triggers minimal ones. Cytokines and other factors derived from keratinocytes play important roles in inflammatory and immune responses in the skin. The authors performed an in vitro investigation to determine the human keratinocyte cytokine profiles during dermatophyte infection. The human keratinocyte cell line PHK16-0b was infected with A. benhamiae or T. tonsurans for 24 h, and the cytokines secreted were analysed using a human cytokine antibody array. Marked differences were observed in the cytokine profiles of the cells infected with the two dermatophytes. A. benhamiae infection resulted in the secretion of a broad spectrum of cytokines, including proinflammatory cytokines, chemokines, and immunomodulatory cytokines. In contrast, T. tonsurans-infected keratinocytes secreted only limited cytokines, including eotaxin-2, interleukin (IL)-8 and IL-16. cDNA microarray analysis confirmed that A. benhamiae infection upregulated genes encoding IL-1beta, IL-2, IL-4, IL-6, IL-10, IL-13, IL-15, IL-16, IL-17 and interferon (IFN)-gamma, while T. tonsurans infection upregulated only a few genes, such as those encoding IL-1beta and IL-16. RT-PCR demonstrated that infection by both dermatophytes enhanced IL-8 mRNA expression in keratinocytes. These results suggest that A. benhamiae-induced secretion of several cytokines from keratinocytes may be involved in a severe inflammatory response, and that the limited cytokine secretion from keratinocytes in response to T. tonsurans infection may result in a minimal inflammatory response in the skin. These cytokine profiles may aid in proving the clinical features of dermatophytosis.
Shiraki
Yumi
Y
Department of Dermatology, Juntendo University School of Medicine, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Ishibashi
Yoshio
Y
Department of Immunobiology, Meiji Pharmaceutical University, Noshio, Kiyose, Tokyo 204-8588, Japan.
Hiruma
Masataro
M
Department of Dermatology and Allergology, Juntendo University Nerima Hospital, Takanodai, Nerima-ku, Tokyo 117-0033, Japan.
Nishikawa
Akemi
A
Department of Immunobiology, Meiji Pharmaceutical University, Noshio, Kiyose, Tokyo 204-8588, Japan.
Ikeda
Shigaku
S
Department of Dermatology, Juntendo University School of Medicine, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
D003883:Arthrodermataceae / Q000276:immunology*; D002460:Cell Line; D016207:Cytokines / Q000096:biosynthesis*; D003881:Dermatomycoses / Q000276:immunology* / Q000382:microbiology*; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D006801:Humans; D015603:Keratinocytes / Q000276:immunology* / Q000382:microbiology; D020411:Oligonucleotide Array Sequence Analysis; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014249:Trichophyton / Q000276:immunology*
D016207:Cytokines; D012333:RNA, Messenger