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Inflammatory Skin Conditions 2017

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2017) | Viewed by 133881

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Prof. Dr. Christopher Jackson

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Sutton Arthritis Research Laboratory, Kolling Institute, University of Sydney at Royal North Shore Hospital, Sydney, Australia
Interests: inflammation; chronic wounds; rheumatoid arthritis; skin; activated protein C; matrix metalloproteinases
Special Issues, Collections and Topics in MDPI journals

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Dear Colleagues,

The skin, the body’s largest organ, provides a barrier to protect the body from environmental insults including pathogens, maintaining temperature and control evaporation. This barrier is located in the outer layer of the skin known as the epidermis, which sits on the dermis. The epidermis is composed mainly of proliferating keratinocytes in the basal layer which differentiate as they migrate outwards to become lipid-bearing corneocytes. Breaches of this barrier are common events, however, the inability to restore this barrier function can result in health problems such as inflammatory skin conditions which are very common and have high morbidity. This group of diseases includes (in approximate increasing order of severity) : acne, which affects 50% of teenagers; rosacea which affects 10% of adults; atopic dermatitis which affects up to 20% population; psoriasis which affects 2%–3% population; chronic wounds which affect <1% population and the devastating, often fatal, toxic epidermal necrolysis, which is rare. New and innovative drugs that dampen inflammation and restore the defective barrier are required to alleviate these recalcitrant conditions.

This Special Issue calls for original research, mini and full reviews, and perspectives that address the progress and current knowledge in the overlapping research topics of inflammatory skin conditions. These include, but are not limited to the fields that are mentioned in the keywords.

Prof. Dr. Chris Jackson
Guest Editor

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Keywords

inflammatory skin conditions
chronic wounds
psoriasis
dermatitis
epidermis
keratinocytes
barrier function
inflammatory cells
immunity

Related Special Issue

Inflammatory Skin Conditions 2020 in International Journal of Molecular Sciences (10 articles)

Published Papers (13 papers)

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Research

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2373 KiB

Open AccessArticle

Human Skin Permeation Studies with PPARγ Agonist to Improve Its Permeability and Efficacy in Inflammatory Processes

by Marcelle Silva-Abreu, Lupe Carolina Espinoza, María José Rodríguez-Lagunas, María-José Fábrega, Marta Espina, María Luisa García and Ana Cristina Calpena

Int. J. Mol. Sci. 2017, 18(12), 2548; https://doi.org/10.3390/ijms18122548 - 28 Nov 2017

Cited by 22 | Viewed by 4645

Abstract

Rosacea is the most common inflammatory skin disease. It is characterized by erythema, inflammatory papules and pustules, visible blood vessels, and telangiectasia. The current treatment has limitations and unsatisfactory results. Pioglitazone (PGZ) is an agonist of peroxisome proliferator-activated receptors (PPARs), a nuclear receptor that regulates important cellular functions, including inflammatory responses. The purpose of this study was to evaluate the permeation of PGZ with a selection of penetration enhancers and to analyze its effectiveness for treating rosacea. The high-performance liquid chromatography (HPLC) method was validated for the quantitative determination of PGZ. Ex vivo permeation experiments were realized in Franz diffusion cells using human skin, in which PGZ with different penetration enhancers were assayed. The results showed that the limonene was the most effective penetration enhancer that promotes the permeation of PGZ through the skin. The cytotoxicity studies and the Draize test detected cell viability and the absence of skin irritation, respectively. The determination of the skin color using a skin colorimetric probe and the results of histopathological studies confirmed the ability of PGZ-limonene to reduce erythema and vasodilation. This study suggests new pharmacological indications of PGZ and its possible application in the treatment of skin diseases, namely rosacea. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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2327 KiB

Open AccessArticle

Effect of Different Skin Penetration Promoters in Halobetasol Propionate Permeation and Retention in Human Skin

by Paulina Carvajal-Vidal, Mireia Mallandrich, María Luisa García and Ana Cristina Calpena

Int. J. Mol. Sci. 2017, 18(11), 2475; https://doi.org/10.3390/ijms18112475 - 21 Nov 2017

Cited by 12 | Viewed by 9075

Abstract

Halobetasol propionate (HB) is a potent synthetic corticosteroid used against inflammatory skin diseases, such as dermatitis, eczema, and psoriasis, among others. The aim of this study is to define how the presence of different skin penetration enhancers (nonane, menthone, limonene, azone, carene, decanol, linoleic acid and cetiol) affects the penetration and retention in skin of HB. To determine drug penetration through skin, 5% of each promoter was used in an ex vivo system with human skin on Franz cells. The results showed that the highest permeation occurs in the presence of menthone, followed by nonane. Permeation parameters were determined. The in vivo test was assessed, and the formulation containing HB-menthone presented better anti-inflammatory efficacy. These results are useful to generate a specific treatment according to each patient’s needs, and the inflammatory characteristics of the disease. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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The MEK Inhibitors Trametinib and Cobimetinib Induce a Type I Interferon Response in Human Keratinocytes

by Daniela Lulli, Maria Luigia Carbone and Saveria Pastore

Int. J. Mol. Sci. 2017, 18(10), 2227; https://doi.org/10.3390/ijms18102227 - 24 Oct 2017

Cited by 25 | Viewed by 7774

Abstract

Mitogen-activated protein kinase kinases (MEK) 1 and 2 have crucial roles in tumorigenesis, cell proliferation, and protection from apoptosis, and their inhibition is therefore an attractive therapeutic strategy in cancer. Orally available and highly selective MEK inhibitors have been developed and assessed in numerous clinical trials, either alone or in combination with cytotoxic chemotherapy and/or other targeted agents. Of note, a complex picture of class-specific adverse effects associates with these drugs, frequently including inflammatory skin rash. Here, we investigated the response of normal human keratinocytes to the MEK inhibitors trametinib and cobimetinib, alone and in combination with the v-Raf murine sarcoma viral oncogene homolog B (BRAF) inhibitors dabrafenib and vemurafenib, in terms of signal transduction and de novo gene expression. MEK inhibitors triggered enhanced expression of interferon regulatory factor 1 (IRF1) and phosphorylation of signal transducer and activator of transcription 1 (STAT1), and up-regulated the keratinocyte-specific type I interferon κ (IFN-κ), the anti-viral effectors interferon-induced tetratricopeptide repeats (IFIT) 1 and 2, and the pro-inflammatory chemokine (C-C motif) ligand 2 (CCL2) and the C-X-C motif chemokine 10 (CXCL10), both at the mRNA and protein level. Impairment of IRF1 expression, or abrogation of STAT1 phosphorylation due to IFN-κ gene silencing, suppressed anti-viral and pro-inflammatory gene expression. These data suggest that, similar to what we observed for epidermal growth factor receptor (EGFR) blockade, MEK inhibition activates a type I interferon response, which is now recognized as an effective anti-cancer response, in human epidermal keratinocytes. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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Open AccessArticle

Antioxidant Artemisia princeps Extract Enhances the Expression of Filaggrin and Loricrin via the AHR/OVOL1 Pathway

by Akiko Hirano, Masashi Goto, Tsukasa Mitsui, Akiko Hashimoto-Hachiya, Gaku Tsuji and Masutaka Furue

Int. J. Mol. Sci. 2017, 18(9), 1948; https://doi.org/10.3390/ijms18091948 - 11 Sep 2017

Cited by 39 | Viewed by 7658

Abstract

The Japanese mugwort, Artemisia princeps (yomogi in Japanese), has anti-inflammatory and antioxidant effects. Skin care products containing Artemisia princeps extract (APE) are known to improve dry skin symptoms in atopic dermatitis. Atopic dry skin is associated with a marked reduction of skin barrier proteins, such as filaggrin (FLG) and loricrin (LOR). Recently, aryl hydrocarbon receptor (AHR), and its downstream transcription factor OVO-like 1 (OVOL1), have been shown to regulate the gene expression of FLG and LOR. The focus of this paper is to evaluate the effects of APE on the AHR/OVOL1/FLG or LOR pathway since they have remained unknown to this point. We first demonstrated that non-cytotoxic concentrations of APE significantly upregulated antioxidant enzymes, NAD(P)H dehydrogenase quinone 1 and heme oxygenase 1, in human keratinocytes. Even at these low concentrations, APE induced nuclear translocation of AHR and significantly upregulated CYP1A1 (a specific target gene for AHR activation), FLG, and LOR expression. AHR knockdown downregulated OVOL1 expression. The APE-induced upregulation of FLG and LOR was canceled in keratinocytes with AHR or OVOL1 knockdown. In conclusion, antioxidant APE is a potent phytoextract that upregulates FLG and LOR expression in an AHR/OVOL1-dependent manner and this may underpin the barrier-repairing effects of APE in treating atopic dry skin. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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Open AccessArticle

The Herbal Bitter Drug Gentiana lutea Modulates Lipid Synthesis in Human Keratinocytes In Vitro and In Vivo

by Ute Wölfle, Birgit Haarhaus, Jasmin Seiwerth, Anja Cawelius, Kay Schwabe, Karl-Werner Quirin and Christoph M. Schempp

Int. J. Mol. Sci. 2017, 18(8), 1814; https://doi.org/10.3390/ijms18081814 - 22 Aug 2017

Cited by 30 | Viewed by 6816

Abstract

Gentiana lutea is a herbal bitter drug that is used to enhance gastrointestinal motility and secretion. Recently we have shown that amarogentin, a characteristic bitter compound of Gentiana lutea extract (GE), binds to the bitter taste receptors TAS2R1 and TAS2R38 in human keratinocytes, and stimulates the synthesis of epidermal barrier proteins. Here, we wondered if GE also modulates lipid synthesis in human keratinocytes. To address this issue, human primary keratinocytes were incubated for 6 days with GE. Nile Red labeling revealed that GE significantly increased lipid synthesis in keratinocytes. Similarly, gas chromatography with flame ionization detector indicated that GE increases the amount of triglycerides in keratinocytes. GE induced the expression of epidermal ceramide synthase 3, but not sphingomyelinase. Lipid synthesis, as well as ceramide synthase 3 expression, could be specifically blocked by inhibitors of the p38 MAPK and PPARγ signaling pathway. To assess if GE also modulates lipid synthesis in vivo, we performed a proof of concept half side comparison on the volar forearms of 33 volunteers. In comparison to placebo, GE significantly increased the lipid content of the treated skin areas, as measured with a sebumeter. Thus, GE enhances lipid synthesis in human keratinocytes that is essential for building an intact epidermal barrier. Therefore, GE might be used to improve skin disorders with an impaired epidermal barrier, e.g., very dry skin and atopic eczema. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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Review

Jump to: Research

27 pages, 912 KiB

Open AccessReview

Role of the IL-23/IL-17 Axis in Psoriasis and Psoriatic Arthritis: The Clinical Importance of Its Divergence in Skin and Joints

by Marie-Astrid Boutet, Alessandra Nerviani, Gabriele Gallo Afflitto and Costantino Pitzalis

Int. J. Mol. Sci. 2018, 19(2), 530; https://doi.org/10.3390/ijms19020530 - 09 Feb 2018

Cited by 141 | Viewed by 21389

Abstract

Psoriasis is a chronic systemic inflammatory disease causing erythematosus and scaly skin plaques; up to 30% of patients with psoriasis develop Psoriatic Arthritis (PsA), which is characterised by inflammation and progressive damage of the peripheral joints and/or the spine and/or the entheses. The pathogenic mechanisms driving the skin disorder in psoriasis and the joint disease in PsA are sustained by the activation of inflammatory pathways that can be overlapping, but also, at least partially, distinct. Cytokines members of the IL-23/IL-17 family, critical in the development of autoimmunity, are abundantly expressed within the cutaneous lesions but also seem to be involved in chronic inflammation and damage of the synovium though, as it will be here discussed, not in all patients. In this review, we will focus on the state of the art of the molecular features of psoriatic skin and joints, focusing on the specific role of the IL-23/IL-17 pathway in each of these anatomical districts. We will then offer an overview of the approved and in-development biologics targeting this axis, emphasising how the availability of the “target” in the diseased tissues could provide a plausible explanation for the heterogeneous clinical efficacy of these drugs, thus opening future perspective of personalised therapies. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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14 pages, 2583 KiB

Open AccessReview

Psoriasis: A STAT3-Centric View

by Enzo Calautti, Lidia Avalle and Valeria Poli

Int. J. Mol. Sci. 2018, 19(1), 171; https://doi.org/10.3390/ijms19010171 - 06 Jan 2018

Cited by 144 | Viewed by 8623

Abstract

Signal Transducer and Activator of Transcription (STAT)3 has recently emerged as a key player in the development and pathogenesis of psoriasis and psoriatic-like inflammatory conditions. Indeed, STAT3 hyperactivation has been reported in virtually every cell type involved in disease initiation and maintenance, and this factor mediates the signal of most cytokines that are involved in disease pathogenesis, including the central Interleukin (IL)-23/IL-17/IL-22 axis. Despite the recent availability of effective biological agents (monoclonal antibodies) against IL-17 and IL-23, which have radically changed the current standard of disease management, the possibility of targeting either STAT3 itself or, even better, the family of upstream activators Janus kinases (JAK1, 2, 3, and TYK2) offers additional therapeutic options. Due to the oral/topical administration modality of these small molecule drugs, their lower cost, and the reduced risk of eliciting adverse immune responses, these compounds are being actively scrutinized in clinical settings. Here, we summarize the main pathological features of psoriatic conditions that provide the rationale for targeting the JAK/STAT3 axis in disease treatment. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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813 KiB

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The Origin of Skin Dendritic Cell Network and Its Role in Psoriasis

by Tae-Gyun Kim, Sung Hee Kim and Min-Geol Lee

Int. J. Mol. Sci. 2018, 19(1), 42; https://doi.org/10.3390/ijms19010042 - 23 Dec 2017

Cited by 30 | Viewed by 10585

Abstract

Dendritic cells (DCs) are heterogeneous groups of innate immune cells, which orchestrate immune responses by presenting antigens to cognate T cells and stimulating other types of immune cells. Although the term ‘DCs’ generally represent highly mixed subsets with functional heterogeneity, the classical definition of DCs usually denotes conventional DCs (cDCs). Skin contains a unique DC network mainly composed of embryo precursor-derived epidermal Langerhans cells (LCs) and bone marrow-derived dermal cDCs, which can be further classified into type 1 (cDC1) and type 2 (cDC2) subsets. Psoriasis is a chronic inflammatory skin disease, which is principally mediated by IL-23/IL-17 cytokine axis. In the psoriatic skins, DCs are prominent cellular sources for TNF-α and IL-23, and the use of blocking antibodies against TNF-α and IL-23 leads to a significant clinical improvement in psoriatic patients. Recent elegant human and mouse studies have shown that inflammation-induced inflammatory DCs, LCs, dermal cDC2, and monocyte-derived DCs are pivotal DC subsets in psoriatic inflammation. Thus, targeting specific pathogenic DC subsets would be a potential strategy for alleviating and preventing DC-derived IL-23-dependent psoriatic inflammation and other inflammatory dermatoses in the future. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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Open AccessReview

Molecular Mechanisms and Management of a Cutaneous Inflammatory Disorder: Psoriasis

by Yu Ri Woo, Dae Ho Cho and Hyun Jeong Park

Int. J. Mol. Sci. 2017, 18(12), 2684; https://doi.org/10.3390/ijms18122684 - 11 Dec 2017

Cited by 81 | Viewed by 9458

Abstract

Psoriasis is a complex chronic inflammatory cutaneous disorder. To date, robust molecular mechanisms of psoriasis have been reported. Among diverse aberrant immunopathogenetic mechanisms, the current model emphasizes the role of Th1 and the IL-23/Th17 axis, skin-resident immune cells and major signal transduction pathways involved in psoriasis. The multiple genetic risk loci for psoriasis have been rapidly revealed with the advent of a novel technology. Moreover, identifying epigenetic modifications could bridge the gap between genetic and environmental risk factors in psoriasis. This review will provide a better understanding of the pathogenesis of psoriasis by unraveling the complicated interplay among immunological abnormalities, genetic risk foci, epigenetic modification and environmental factors of psoriasis. With advances in molecular biology, diverse new targets are under investigation to manage psoriasis. The recent advances in treatment modalities for psoriasis based on targeted molecules are also discussed. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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1746 KiB

Open AccessReview

Adjuvant Biological Therapies in Chronic Leg Ulcers

by Natalia Burgos-Alonso, Igone Lobato, Igone Hernández, Kepa San Sebastian, Begoña Rodríguez, Gontzal Grandes and Isabel Andia

Int. J. Mol. Sci. 2017, 18(12), 2561; https://doi.org/10.3390/ijms18122561 - 28 Nov 2017

Cited by 18 | Viewed by 5072

Abstract

Current biological treatments for non-healing wounds aim to address the common deviations in healing mechanisms, mainly inflammation, inadequate angiogenesis and reduced synthesis of extracellular matrix. In this context, regenerative medicine strategies, i.e., platelet rich plasmas and mesenchymal stromal cell products, may form part of adjuvant interventions in an integral patient management. We synthesized the clinical experience on ulcer management using these two categories of biological adjuvants. The results of ten controlled trials that are included in this systematic review favor the use of mesenchymal stromal cell based-adjuvants for impaired wound healing, but the number and quality of studies is moderate-low and are complicated by the diversity of biological products. Regarding platelet-derived products, 18 controlled studies investigated their efficacy in chronic wounds in the lower limb, but the heterogeneity of products and protocols hinders clinically meaningful quantitative synthesis. Most patients were diabetic, emphasizing an unmet medical need in this condition. Overall, there is not sufficient evidence to inform routine care, and further clinical research is necessary to realize the full potential of adjuvant regenerative medicine strategies in the management of chronic leg ulcers. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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3802 KiB

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Paraneoplastic Pemphigus: Insight into the Autoimmune Pathogenesis, Clinical Features and Therapy

by Giovanni Paolino, Dario Didona, Giuseppe Magliulo, Giannicola Iannella, Biagio Didona, Santo Raffaele Mercuri, Elisa Moliterni, Michele Donati, Andrea Ciofalo, Guido Granata, Patricia Ranuzzi, Vincenzo Falasca and Stefano Calvieri

Int. J. Mol. Sci. 2017, 18(12), 2532; https://doi.org/10.3390/ijms18122532 - 26 Nov 2017

Cited by 86 | Viewed by 15816

Abstract

Paraneoplastic pemphigus is a rare autoimmune skin disease that is always associated with a neoplasm. Usually, oral, skin, and mucosal lesions are the earliest manifestations shown by paraneoplastic pemphigus patients. The pathogenesis of paraneoplastic pemphigus is not yet completely understood, although some immunological aspects have been recently clarified. Because of its rarity, several diagnostic criteria have been proposed. Besides, several diagnostic procedures have been used for the diagnosis, including indirect immunofluorescence, direct immunofluorescence, and ELISA. We reviewed the most recent literature, searching on PubMed “paraneoplastic pemphigus”. We included also papers in French, German, and Spanish. We found 613 papers for “paraneoplastic pemphigus”. Among them, 169 were review papers. Because of its varying clinical features, paraneoplastic pemphigus still represents a challenge for clinicians. Furthermore, diagnosis and management of paraneoplastic pemphigus requires close collaboration between physicians, including dermatologist, oncologist, and otorhinolaryngologist. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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Inflammatory and Noninflammatory Itch: Implications in Pathophysiology-Directed Treatments

by Lai-San Wong, Tiffany Wu and Chih-Hung Lee

Int. J. Mol. Sci. 2017, 18(7), 1485; https://doi.org/10.3390/ijms18071485 - 10 Jul 2017

Cited by 26 | Viewed by 6457

Abstract

Itch is the main chief complaint in patients visiting dermatologic clinics and has the ability to deeply impair life quality. Itch results from activation of cutaneous nerve endings by noxious stimuli such as inflammatory mediators, neurotransmitters and neuropeptides, causing itch signal transduction from peripheral skin, through the spinal cord and thalamus, to the brain cortex. Primarily noninflammatory diseases, such as uremic pruritus, cause itch through certain pruritogens in the skin. In inflammatory skin diseases, atopic dermatitis (AD) is the prototypic disease causing intensive itch by aberrant skin inflammation and epidermal barrier disruption. Recent understanding of disease susceptibility, severity markers, and mechanisms have helped to develop targeted therapy for itch in AD, including monoclonal antibodies against IL-4, IL-13, thymic stromal lymphopoietin (TSLP), IgE and IL-31. Promising effects have been observed in some of them. In this review, we summarized targeted therapies for inflammatory itch in AD and for managing abnormal itch transductions in other common itching skin diseases. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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1978 KiB

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Cutaneous Manifestations of Human and Murine Leishmaniasis

by Breanna M. Scorza, Edgar M. Carvalho and Mary E. Wilson

Int. J. Mol. Sci. 2017, 18(6), 1296; https://doi.org/10.3390/ijms18061296 - 18 Jun 2017

Cited by 141 | Viewed by 19374

Abstract

The leishmaniases are diseases caused by pathogenic protozoan parasites of the genus Leishmania. Infections are initiated when a sand fly vector inoculates Leishmania parasites into the skin of a mammalian host. Leishmania causes a spectrum of inflammatory cutaneous disease manifestations. The type of cutaneous pathology is determined in part by the infecting Leishmania species, but also by a combination of inflammatory and anti-inflammatory host immune response factors resulting in different clinical outcomes. This review discusses the distinct cutaneous syndromes described in humans, and current knowledge of the inflammatory responses associated with divergent cutaneous pathologic responses to different Leishmania species. The contribution of key hematopoietic cells in experimental cutaneous leishmaniasis in mouse models are also reviewed and compared with those observed during human infection. We hypothesize that local skin events influence the ensuing adaptive immune response to Leishmania spp. infections, and that the balance between inflammatory and regulatory factors induced by infection are critical for determining cutaneous pathology and outcome of infection. Full article

(This article belongs to the Special Issue Inflammatory Skin Conditions 2017)

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