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Interleukin-6 and the Lung
Published in Jason Kelley, Cytokines of the Lung, 2022
Ralph J. Zitnik, Jack A. Elias
Psoriasis is characterized by excessive proliferation of keratinocytes as well as dermal and epidermal infiltration by inflammatory cells. Grossman et al. (1989) demonstrated that patients with psoriasis have elevated serum levels of IL-6; increased immunologically detectable IL-6 in the epidermis, dermis, and endothelial cells of psoriatic placques; and increased levels of IL-6 mRNA and IL-6 protein in areas of psoriatic involvement. Keratinocytes from psoriatic plaques produce IL-6 and proliferate in response to IL-6, suggesting that autocrine effects of IL-6 are involved in this disorder. However, Prens et al. (1990) were unable to demonstrate IL-6 staining within psoriatic lesions or on cultured keratinocytes. They did note abnormally large amounts of steady-state IL-6 mRNA in psoriatic fibroblasts. These disorders suggest that IL-6 is involved in the pathogenesis of psoriasis. However, additional investigation will be required to finally establish the role that IL-6 plays in this disorder and to determine the cell or cells responsible for the abnormal IL-6 production in these patients.
Benign Neoplasms
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Abdullah Demirbaş, Ömer Faruk Elmas, Necmettin Akdeniz
Overview: This represents a benign patch of darkened skin. It results from exposure to UV light, which induces local melanocyte proliferation and melanin aggregation in the keratinocytes. Solar lentigines are very common, especially in people older than 40 years of age.
Exploring the Plant Kingdom for Sources of Skincare Cosmeceuticals
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Wild Plants, 2020
Mayuri Napagoda, Sanjeeva Witharana
Skin color is primarily determined by the amount of melanin present in the skin. Melanin is a pigment produced by melanocytes through a process known as melanogenesis, from which the amino acid L-tyrosine gets converted by the enzyme tyrosinase into dopaquinone (Cooksey et al. 1997). Although melanogenesis and skin pigmentation are considered as natural photoprotective approaches in response to UV-induced skin photocarcinogenesis, the increased melanin synthesis and accumulation of these pigments give rise to many aesthetic and dermatological problems, such as melasma, periorbital hyperpigmentation, freckles, or lentigines (Smit et al. 2009, Zolghadri et al. 2019). Pigmentation is either dependent on the number, size, composition, and distribution of melanocytes, or activity of melanogenic enzymes. Furthermore, cutaneous pigmentation is resulted from melanin synthesis by melanocytes and transfer of melanosome to keratinocytes (Lin et al. 2008).
Exposure to the anti-microbial chemical triclosan disrupts keratinocyte function and skin integrity in a model of reconstructed human epidermis
Published in Journal of Immunotoxicology, 2023
Rachel Baur, Michael Kashon, Ewa Lukomska, Lisa M. Weatherly, Hillary L. Shane, Stacey E. Anderson
Keratinocytes are key players in the structural integrity of the skin and they are involved in sensing and reacting to the environment (Hammad and Lambrecht 2015). Cytokine signaling is a key mechanism that keratinocytes use to interact with immune cells, both by producing cyto-kines and responding to cytokines via cytokine receptors (Hammad and Lambrecht 2015; Jiang et al. 2020). Certain cytokines that are produced by epithelial cells including keratinocytes, such as thymic stromal lymphopoietin (TSLP), IL-25, and IL-33, can communicate with immune cells and skew immune responses toward T-helper cell Type 2 (TH2) responses, leading to increased risk of sensitization (Hammad and Lambrecht 2015; Goleva et al. 2019). Dermal exposure to triclosan has been shown to increase levels of Tslp, as well as other signaling molecules such as S100 calcium-binding protein A8 (S100a8), IL-1β (Il1b), chemokine (C-X-C motif) ligand (Cxcl)1, and Cxcl2 in mouse skin (Anderson et al. 2020; Weatherly et al. 2020). Additionally, triclosan exposure on mouse skin has been shown to alter expression of filaggrin and keratin genes, demonstrating an impact on keratinocytes (Baur et al. 2021). Exposure to triclosan on human keratinocytes in vitro has been shown to alter metabolic pathways and increase pro-inflammatory cytokines (Liang et al. 2021). However, the impact of triclosan exposure on human keratinocyte response and the skin barrier is not well understood.
Occupational exposure assessment with solid substances: choosing a vehicle for in vitro percutaneous absorption experiments
Published in Critical Reviews in Toxicology, 2022
Catherine Champmartin, Lisa Chedik, Fabrice Marquet, Frédéric Cosnier
As shown in Figure 1, the epidermis is a coating epithelium. The viable epidermis, with a thickness varying roughly from 30 to 100 µm, consists of the stratum basale, the stratum spinosum, and the stratum granulosum (SG). It is separated from the dermis by the basement membrane. The viable epidermis is innervated but not vascularized, and its nutritional needs are met through diffusion from the basement membrane. One of its functions is as a barrier against environmental aggression. The majority (80%) of epidermal cells are the keratinocytes; the other cell types found in the epidermis are melanocytes, Langerhans cells, and Merkel cells. Specialized junctions called corneodesmosomes or desmosomes (to which the tonofilaments are tethered) (Prost-Squarcioni 2006) link keratinocytes together and contribute to the outside-in epidermal barrier. The highly protective outermost layer of the epidermis – the stratum corneum (SC) – is constantly renewed. It is about 10–40 µm thick and composed of 15–25 layers of corneocytes, i.e. dead and keratinized cells resulting from the terminal differentiation of keratinocytes that have migrated to the skin’s surface.
Miconazole and terbinafine induced reactive oxygen species accumulation and topical toxicity in human keratinocytes
Published in Drug and Chemical Toxicology, 2022
P.-L. Lam, M.-M. Wong, L.-K. Hung, L.-H. Yung, J. C.-O. Tang, K.-H. Lam, P.-Y. Chung, W.-Y. Wong, Y.-W. Ho, R. S.-M. Wong, R. Gambari, C.-H. Chui
This raises a question on the impact of ROS-inducing antimycotic drugs (i.e., miconazole and terbinafine) on skin wound healing, considering that the generation of ROS can cause topical toxicity. We hypothesized that miconazole and terbinafine have anti-wound healing effects on skin cells when used in antifungal treatment because they have been recently demonstrated to have a strong ability to generate ROS. Therefore, they are believed to inhibit fungal growth via the inhibition of ergosterol synthesis, and owing to the ability of miconazole and terbinafine to produce ROS in fungi, we suspect that when used topically, they may also stimulate ROS generation in skin cells. Of note, keratinocytes are the predominant cell type in the epidermis (Jang et al.2017, Bhushan et al.2019) and are fundamental to the structural and barrier functions of the epidermis (Kim et al.2018, Choi et al.2019). To the best of our knowledge, the effect of miconazole and terbinafine on HaCaT cells (an immortalized human keratinocyte line) has not been studied previously with respect to intracellular ROS stimulation. Thus, in this study, we aimed to investigate whether miconazole and terbinafine exert anti-wound healing effects on HaCaT cells.