Cytokine secretion profiles of human keratinocytes during Trichophyton tonsurans and Arthroderma benhamiae infections

Abstract

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-1β, IL-2, IL-4, IL-6, IL-10, IL-13, IL-15, IL-16, IL-17 and interferon (IFN)-γ, while T. tonsurans infection upregulated only a few genes, such as those encoding IL-1β 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.

Procathepsin D secreted by HaCaT keratinocyte cells – A novel regulator of keratinocyte growth

“…The group of cytokines secreted includes IL-4, IL-6, IL-8, IL-10, IL-13, and MIP-1β. The expression of 6,8,10, and 13 has been observed in keratinocytes under pathological conditions as an inflammatory response (Shiraki et al, 2006). The increased expression of IL-6 and IL-8 has been shown in a murine wound healing model (Bryan et al, 2005).…”

Dermatófitos: interação patógeno-hospedeiro e resistência a antifúngicos

“…It was shown that Arthroderma benhamiae, a zoophilic dermatophyte and teleomorph of T. mentagrophytes, induces the expression of various cytokines by keratinocytes, which may be involved in the development of an inflammatory response, typical of these infections. 33 Nevertheless, the authors affirm that these cells, when in contact with T. tonsurans, an anthropophilic dermatophyte, showed a limited cytokine expression, which probably explains the low inflammatory response provoked in lesions caused by this species. Other authors also described a difference in the profile of cytokine expression by keratinocytes infected in vitro by T. mentagrophytes, T. rubrum and T. tonsurans, which would also explain the difference in the intensity of induced inflammatory responses during infection by these species.…”

Expression of CD1d and Ligand-Induced Cytokine Production Are Tissue Specific in Mucosal Epithelia of the Human Lower Reproductive Tract

“…Activation of CD1d-restricted invariant NKT (iNKT) cells enhances host resistance to some microbes in a manner dependent on the level of CD1d expression on APCs (29,30). In contrast, the activation of iNKT cells promotes susceptibility to some microbes (3,28). For instance, in the murine lung, the immune responses of iNKT cells to two very closely related microbes, Chlamydia pneumoniae and Chlamydia muridarum, are protective and harmful, respectively (19).…”

“…Intracellular signaling mediated by surface CD1d utilizes NF-B, a well-known immune-related transcription factor (32,38). CD1d-restricted NKT cells can act directly on infected cells, killing CD1d-expressing cells (28). They can also modulate adaptive immune cells by altering Th1-Th2 polarization.…”