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Cells
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Skin Defense against Oxidative Stress and Inflammation
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Skin Defense against Oxidative Stress and Inflammation

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (30 August 2021) | Viewed by 23224

Special Issue Editor

Prof. Dr. Gabriella Fabbrocini

E-Mail Website
Guest Editor
Section of Dermatology, Department of Clinical Medicine and Surgery, University of Naples Federico II, 80131 Napoly, Italy
Interests: acne; inflammatory skin diseases (atopic dermatitis; hidradenitis; psoriasis); dermoscopy; melanoma; photodermatology and alopecia; dermocosmetological care of chemotherapy skin reaction “corpo ritrovato”
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress is an imbalance between oxidants and antioxidants in favour of the oxidants, leading to a disruption of redox signalling and control and/or molecular damage. Reactive oxygen species mediated oxidative damage involves a vast number of biological molecules since it causes lipid peroxidation, DNA modification, and the secretion of inflammatory cytokines. The cellular redox balance is tightly regulated by several (enzymatic) antioxidants and pro-oxidants. An imbalance in this pathway induces an aberrant inflammatory response. On the other hand, if physiological inflammation is essential for the protection against injurious insults, chronic and pathological inflammation can result in an aberrant response with additional tissue damage, generating an abnormal oxidative stress overload and resulting in cellular damage, triggering a vicious circle.

Both oxidative stress and aberrant inflammation play a relevant role in the pathophysiology of several chronic skin diseases, as well as in skin aging.

Crucially, data from literture point to modulation of oxidative stress and inflammation as an effective therapy to prevent or cure several cutaneous pathological situations.

The aim of this Special Issue is to provide a special focus on model organisms and in vitro mammalian systems used to study the regulation, mechanisms and functions of oxidative stress and inflammation. We hope that the data presented in this issue will help the community of researchers in dermatology investigating oxidative stress and inflammation in different skin diseases.

Prof. Gabriella Fabbrocini
Guest Editor

Keywords

  • oxidative stress
  • inflammation
  • skin diseases
  • biomarkers
  • in vivo
  • ex vivo
  • skin aging

Published Papers (3 papers)

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Research

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16 pages, 4532 KiB  
Article
Herb Sanqi-Derived Compound K Alleviates Oxidative Stress in Cultured Human Melanocytes and Improves Oxidative-Stress-Related Leukoderma in Guinea Pigs
by Suwei Tang, Lingli Yang, Yasutaka Kuroda, Sylvia Lai, Shaoqiong Xie, Huimin Zhang and Ichiro Katayama
Cells 2021, 10(8), 2057; https://doi.org/10.3390/cells10082057 - 11 Aug 2021
Cited by 4 | Viewed by 2387
Abstract
Sanqi, a traditional Chinese herb, is widely used for cardiovascular diseases, and its neuroprotective effects against oxidative stress were recently discovered. The purpose of this study was to investigate whether Sanqi-derived compound K (Sanqi-CK), an active metabolite of Sanqi, could protect melanocytes from [...] Read more.
Sanqi, a traditional Chinese herb, is widely used for cardiovascular diseases, and its neuroprotective effects against oxidative stress were recently discovered. The purpose of this study was to investigate whether Sanqi-derived compound K (Sanqi-CK), an active metabolite of Sanqi, could protect melanocytes from oxidative stress. Cultured human primary skin epidermal melanocytes (HEMn-MPs) were treated with hydrogen peroxide (H2O2) in the presence or absence of Sanqi-CK. Sanqi-CK exhibited protective effects against H2O2-induced cell death by reducing oxidative stress. In addition, treatment with Sanqi-CK reversed the decreased glutathione reductase activity and decreased ratio of reduced glutathione (GSH)/oxidized glutathione (GSSG) seen in H2O2-treated melanocytes. Furthermore, topical application of Sanqi-CK alleviated leukoderma in guinea pigs, a disorder characterized by melanocyte cell death resulting from rhododendrol-induced oxidative stress. Taken together, these data suggest that Sanqi-CK protects melanocytes against oxidative stress, and its protective effects are associated with modulating the redox balance between GSH and GSSG and activating glutathione reductase. Thus, Sanqi-CK may be a good candidate for preventing melanocyte loss in oxidative-stress-associated pigmentary disorders. Full article
(This article belongs to the Special Issue Skin Defense against Oxidative Stress and Inflammation)
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14 pages, 1901 KiB  
Article
Keratinocytes Regulate the Threshold of Inflammation by Inhibiting T Cell Effector Functions
by Peter Seiringer, Stefanie Eyerich, Kilian Eyerich, Daniela Dittlein, Anna Caroline Pilz, Emanuele Scala, Johannes Ring, Heidrun Behrendt, Andrea Cavani and Claudia Traidl-Hoffmann
Cells 2021, 10(7), 1606; https://doi.org/10.3390/cells10071606 - 26 Jun 2021
Cited by 6 | Viewed by 2387
Abstract
Whilst the importance of keratinocytes as a first-line defense has been widely investigated, little is known about their interactions with non-resident immune cells. In this study, the impact of human keratinocytes on T cell effector functions was analyzed in an antigen-specific in vitro [...] Read more.
Whilst the importance of keratinocytes as a first-line defense has been widely investigated, little is known about their interactions with non-resident immune cells. In this study, the impact of human keratinocytes on T cell effector functions was analyzed in an antigen-specific in vitro model of allergic contact dermatitis (ACD) to nickel sulfate. Keratinocytes partially inhibited T cell proliferation and cytokine production. This effect was dependent on the keratinocyte/T cell ratio and was partially reversible by increasing the number of autologous dendritic cells. The inhibition of T cell proliferation by keratinocytes was independent of the T cell subtype and antigen presentation by different professional antigen-presenting cells. Autologous and heterologous keratinocytes showed comparable effects, while the fixation of keratinocytes with paraformaldehyde abrogated the immunosuppressive effect. The separation of keratinocytes and T cells by a transwell chamber, as well as a cell-free keratinocyte supernatant, inhibited T cell effector functions to the same amount as directly co-cultured keratinocytes, thus proving that soluble factor/s account for the observed suppressive effects. In conclusion, keratinocytes critically control the threshold of inflammatory processes in the skin by inhibiting T cell proliferation and cytokine production. Full article
(This article belongs to the Special Issue Skin Defense against Oxidative Stress and Inflammation)
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Review

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19 pages, 1820 KiB  
Review
Hidradenitis Suppurativa: Where We Are and Where We Are Going
by Emanuele Scala, Sara Cacciapuoti, Natalie Garzorz-Stark, Matteo Megna, Claudio Marasca, Peter Seiringer, Thomas Volz, Kilian Eyerich and Gabriella Fabbrocini
Cells 2021, 10(8), 2094; https://doi.org/10.3390/cells10082094 - 15 Aug 2021
Cited by 44 | Viewed by 17638
Abstract
Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease primarily affecting apocrine gland-rich areas of the body. It is a multifactorial disease in which genetic and environmental factors play a key role. The primary defect in HS pathophysiology involves follicular occlusion of the [...] Read more.
Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease primarily affecting apocrine gland-rich areas of the body. It is a multifactorial disease in which genetic and environmental factors play a key role. The primary defect in HS pathophysiology involves follicular occlusion of the folliculopilosebaceous unit, followed by follicular rupture and immune responses. Innate pro-inflammatory cytokines (e.g., IL-1β, and TNF-α); mediators of activated T helper (Th)1 and Th17 cells (e.g., IFN-γ, and IL-17); and effector mechanisms of neutrophilic granulocytes, macrophages, and plasma cells are involved. On the other hand, HS lesions contain anti-inflammatory mediators (e.g., IL-10) and show limited activity of Th22 cells. The inflammatory vicious circle finally results in pain, purulence, tissue destruction, and scarring. HS pathogenesis is still enigmatic, and a valid animal model for HS is currently not available. All these aspects represent a challenge for the development of therapeutic approaches, which are urgently needed for this debilitating disease. Available treatments are limited, mostly off-label, and surgical interventions are often required to achieve remission. In this paper, we provide an overview of the current knowledge surrounding HS, including the diagnosis, pathogenesis, treatments, and existing translational studies. Full article
(This article belongs to the Special Issue Skin Defense against Oxidative Stress and Inflammation)
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