International Journal of Molecular Sciences

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8 pages, 1531 KiB

Open AccessArticle

Increased Serum Levels of Tumor Necrosis Factor-like Ligand 1A in Atopic Dermatitis

by Teruyoshi Hisamoto, Hiraku Suga, Asako Yoshizaki-Ogawa, Shinichi Sato and Ayumi Yoshizaki

Int. J. Mol. Sci. 2023, 24(3), 1813; https://doi.org/10.3390/ijms24031813 - 17 Jan 2023

Cited by 3 | Viewed by 2270

Abstract

Atopic dermatitis (AD) is a common chronic skin disease with pruritus, affecting 5–20% of the population in developed countries. Though its cause varies from genetic polymorphisms to the environmental factors, the T-helper (Th) 2 inflammation is one of the main characteristic pathoses. TNF [...] Read more.

Atopic dermatitis (AD) is a common chronic skin disease with pruritus, affecting 5–20% of the population in developed countries. Though its cause varies from genetic polymorphisms to the environmental factors, the T-helper (Th) 2 inflammation is one of the main characteristic pathoses. TNF superfamily ligand A (TL1A) is a recently discovered cytokine, which is released by various immune cells and reported to have an ability to stimulate Th1, Th2, and Th17 responses. Its association was investigated in chronic inflammatory disease, such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis. However, its role on AD is unclear. To elucidate the association of TL1A in AD, we measured the serum TL1A levels in AD patients and healthy controls and performed the immunohistochemistry of TL1A. The result showed that the serum TL1A levels were higher in AD patients than healthy controls, and they positively correlated with the serum immunoglobulin E levels, serum Lactate dehydrogenase, and the number of eosinophils in peripheral blood. The immunohistochemistry of TL1A also showed TL1A expression in epithelium of AD samples. Because previous studies indicate TL1A has a certain role as an inflammation enhancer in Th2 and/or Th17 polarized disease, TL1A in AD may also has a role as an inflammation generator. Full article

(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities)

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15 pages, 2883 KiB

Open AccessArticle

Increased Expression of Galectin-3 in Skin Fibrosis: Evidence from In Vitro and In Vivo Studies

by Teresa Peiró, Miriam Alonso-Carpio, Pilar Ribera, Patricia Almudéver, Inés Roger, Paula Montero, Severiano Marín, Javier Milara and Julio Cortijo

Int. J. Mol. Sci. 2022, 23(23), 15319; https://doi.org/10.3390/ijms232315319 - 5 Dec 2022

Viewed by 2007

Abstract

Skin fibrosis is a hallmark of a wide array of dermatological diseases which can greatly impact the patients’ quality of life. Galectin-3 (GAL-3) has emerged as a central regulator of tissue fibrosis, playing an important pro-fibrotic role in numerous organs. Various studies are [...] Read more.

Skin fibrosis is a hallmark of a wide array of dermatological diseases which can greatly impact the patients’ quality of life. Galectin-3 (GAL-3) has emerged as a central regulator of tissue fibrosis, playing an important pro-fibrotic role in numerous organs. Various studies are highlighting its importance as a skin fibrotic diseases biomarker; however, there is a need for further studies that clarify its role. This paper aims to ascertain whether the expression of GAL-3 is increased in relevant in vitro and in vivo models of skin fibrosis. We studied the role of GAL-3 in vitro using normal human dermal fibroblasts (NHDF) and fibrocytes. In addition, we used a skin fibrosis murine model (BALB/c mice) and human biopsies of healthy or keloid tissue. GAL-3 expression was analyzed using real time PCR, Western blot and immunostaining techniques. We report a significantly increased expression of GAL-3 in NHDF and fibrocytes cell cultures following stimulation with transforming growth factor β1 (TGFβ1). In vivo, GAL-3 expression was increased in a murine model of systemic sclerosis and in human keloid biopsies. In sum, this study underlines the involvement of GAL-3 in skin fibrosis using several models of the disease and highlights its role as a relevant target. Full article

(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities)

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Review

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22 pages, 1530 KiB

Open AccessReview

Total Skin Treatment with Helical Arc Radiotherapy

by Hsin-Hua Nien, Chen-Hsi Hsieh, Pei-Wei Shueng and Hui-Ju Tien

Int. J. Mol. Sci. 2023, 24(5), 4492; https://doi.org/10.3390/ijms24054492 - 24 Feb 2023

Cited by 1 | Viewed by 2163

Abstract

For widespread cutaneous lymphoma, such as mycosis fungoides or leukemia cutis, in patients with acute myeloid leukemia (AML) and for chronic myeloproliferative diseases, total skin irradiation is an efficient treatment modality for disease control. Total skin irradiation aims to homogeneously irradiate the skin [...] Read more.

For widespread cutaneous lymphoma, such as mycosis fungoides or leukemia cutis, in patients with acute myeloid leukemia (AML) and for chronic myeloproliferative diseases, total skin irradiation is an efficient treatment modality for disease control. Total skin irradiation aims to homogeneously irradiate the skin of the entire body. However, the natural geometric shape and skin folding of the human body pose challenges to treatment. This article introduces treatment techniques and the evolution of total skin irradiation. Articles on total skin irradiation by helical tomotherapy and the advantages of total skin irradiation by helical tomotherapy are reviewed. Differences among each treatment technique and treatment advantages are compared. Adverse treatment effects and clinical care during irradiation and possible dose regimens are mentioned for future prospects of total skin irradiation. Full article

(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities)

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16 pages, 1669 KiB

Open AccessReview

Comprehensive Insight into Lichen Planus Immunopathogenesis

by Marijana Vičić, Nika Hlača, Marija Kaštelan, Ines Brajac, Vlatka Sotošek and Larisa Prpić Massari

Int. J. Mol. Sci. 2023, 24(3), 3038; https://doi.org/10.3390/ijms24033038 - 3 Feb 2023

Cited by 16 | Viewed by 7693

Abstract

Lichen planus is a chronic disease affecting the skin, appendages, and mucous membranes. A cutaneous lichen planus is a rare disease occurring in less than 1% of the general population, while oral illness is up to five times more prevalent; still, both forms [...] Read more.

Lichen planus is a chronic disease affecting the skin, appendages, and mucous membranes. A cutaneous lichen planus is a rare disease occurring in less than 1% of the general population, while oral illness is up to five times more prevalent; still, both forms equally impair the patient’s quality of life. The etiology of lichen planus is not entirely understood. Yet, immune-mediated mechanisms have been recognized since environmental factors such as hepatitis virus infection, mechanical trauma, psychological stress, or microbiome changes can trigger the disease in genetically susceptible individuals. According to current understanding, lichen planus immunopathogenesis is caused by cell-mediated cytotoxicity, particularly cytotoxic T lymphocytes, whose activity is further influenced by Th1 and IL-23/Th-17 axis. However, other immunocytes and inflammatory pathways complement these mechanisms. This paper presents a comprehensive insight into the actual knowledge about lichen planus, with the causal genetic and environmental factors being discussed, the immunopathogenesis described, and the principal effectors of its inflammatory circuits identified. Full article

(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities)

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14 pages, 1116 KiB

Open AccessReview

Is Atopic Dermatitis Only a Skin Disease?

by Alicja Mesjasz, Marta Zawadzka, Maciej Chałubiński and Magdalena Trzeciak

Int. J. Mol. Sci. 2023, 24(1), 837; https://doi.org/10.3390/ijms24010837 - 3 Jan 2023

Cited by 14 | Viewed by 4309

Abstract

Atopic dermatitis (AD) is a chronic, pruritic, inflammatory dermatosis that imposes significant patient and population burdens. In addition to the cutaneous signs and symptoms, growing evidence suggests that AD is systemic in nature. Certain diseases can possibly co-occur with AD as a result [...] Read more.

Atopic dermatitis (AD) is a chronic, pruritic, inflammatory dermatosis that imposes significant patient and population burdens. In addition to the cutaneous signs and symptoms, growing evidence suggests that AD is systemic in nature. Certain diseases can possibly co-occur with AD as a result of coincidental exposure to similar environmental factors. However, it is also suspected that they are linked to the pathogenesis of AD through more complex genetic and immunological mechanisms, but these correlations remain less understood. It is of great need to seek explanations for the higher frequency of the number of cardiovascular, autoimmune, neurological, psychiatric, and metabolic disorders that have been observed in epidemiologic investigations among AD patients. Moreover, analysing the immunology of chronic inflammation and its correction, activation, or suppression may prevent the development of a variety of comorbidities. As comorbid diseases in patients diagnosed with AD may potentially go undetected, physicians should be aware of them. Full article

(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities)

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16 pages, 939 KiB

Open AccessReview

IL-33 and IL-37: A Possible Axis in Skin and Allergic Diseases

by Francesco Borgia, Paolo Custurone, Federica Li Pomi, Mario Vaccaro, Clara Alessandrello and Sebastiano Gangemi

Int. J. Mol. Sci. 2023, 24(1), 372; https://doi.org/10.3390/ijms24010372 - 26 Dec 2022

Cited by 10 | Viewed by 2815

Abstract

Interleukin (IL)-37 and IL-33 are among the latest cytokines identified, playing a role in several inflammatory conditions, spanning from systemic conditions to tumors to localized diseases. As newly discovered interleukins, their role is still scarcely understood, but their potential role as therapeutic targets [...] Read more.

Interleukin (IL)-37 and IL-33 are among the latest cytokines identified, playing a role in several inflammatory conditions, spanning from systemic conditions to tumors to localized diseases. As newly discovered interleukins, their role is still scarcely understood, but their potential role as therapeutic targets or disease activity markers suggests the need to reorganize the current data for a better interpretation. The aim of this review is to collect and organize data produced by several studies to create a complete picture. The research was conducted on the PubMed database, and the resulting articles were sorted by title, abstract, English language, and content. Several studies have been assessed, mostly related to atopic dermatitis and immunologic pathways. Collective data demonstrates a pro-inflammatory role of IL-33 and an anti-inflammatory one for IL-37, possibly related to each other in an IL-33/IL-37 axis. Although further studies are needed to assess the safety and plausibility of targeting these two interleukins for patients affected by skin conditions, the early results indicate that both IL-33 and IL-37 represent markers of disease activity. Full article

(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities)

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14 pages, 1030 KiB

Open AccessReview

Chronic Nodular Prurigo: An Update on the Pathogenesis and Treatment

by Lai-San Wong and Yu-Ta Yen

Int. J. Mol. Sci. 2022, 23(20), 12390; https://doi.org/10.3390/ijms232012390 - 16 Oct 2022

Cited by 8 | Viewed by 6459

Abstract

Chronic nodular prurigo (CNPG) is a recalcitrant chronic itchy disorder that affects the quality of life. It can be triggered by multiple etiologies, such as atopic dermatitis, diabetes, and chronic renal diseases. The mechanisms of CNPG are complicated and involved the interaction of [...] Read more.

Chronic nodular prurigo (CNPG) is a recalcitrant chronic itchy disorder that affects the quality of life. It can be triggered by multiple etiologies, such as atopic dermatitis, diabetes, and chronic renal diseases. The mechanisms of CNPG are complicated and involved the interaction of the cutaneous, immune, and nervous systems. Diverse immune cells, including eosinophils, neutrophils, T cells, macrophages, and mast cells infiltrated the lesional skin of CNPG, which initiated the inflammatory cytokines and pruritogens release. In addition, the interaction between the immune cells and activated peripheral sensory nerve fibers by neurotransmitters caused neuroinflammation in the skin and intractable itch. This itch-scratch vicious cycle of CNPG results in disease exacerbation. CNPG is difficult to treat with traditional therapies. Recently, great advances have been made in the pathophysiology of both inflammation and pruritus transmission in CNPG. In this review, we summarize the updated mechanisms and novel therapies for CNPG. Full article

(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities)

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39 pages, 2510 KiB

Open AccessReview

The Role of Transcription Factor PPAR-γ in the Pathogenesis of Psoriasis, Skin Cells, and Immune Cells

by Vladimir V. Sobolev, Ekaterina Tchepourina, Irina M. Korsunskaya, Natalia A. Geppe, Svetlana N. Chebysheva, Anna G. Soboleva and Alexandre Mezentsev

Int. J. Mol. Sci. 2022, 23(17), 9708; https://doi.org/10.3390/ijms23179708 - 26 Aug 2022

Cited by 19 | Viewed by 2987

Abstract

The peroxisome proliferator-activated receptor PPAR-γ is one of three PPAR nuclear receptors that act as ligand-activated transcription factors. In immune cells, the skin, and other organs, PPAR-γ regulates lipid, glucose, and amino acid metabolism. The receptor translates nutritional, pharmacological, and metabolic stimuli into [...] Read more.

The peroxisome proliferator-activated receptor PPAR-γ is one of three PPAR nuclear receptors that act as ligand-activated transcription factors. In immune cells, the skin, and other organs, PPAR-γ regulates lipid, glucose, and amino acid metabolism. The receptor translates nutritional, pharmacological, and metabolic stimuli into the changes in gene expression. The activation of PPAR-γ promotes cell differentiation, reduces the proliferation rate, and modulates the immune response. In the skin, PPARs also contribute to the functioning of the skin barrier. Since we know that the route from identification to the registration of drugs is long and expensive, PPAR-γ agonists already approved for other diseases may also represent a high interest for psoriasis. In this review, we discuss the role of PPAR-γ in the activation, differentiation, and proliferation of skin and immune cells affected by psoriasis and in contributing to the pathogenesis of the disease. We also evaluate whether the agonists of PPAR-γ may become one of the therapeutic options to suppress the inflammatory response in lesional psoriatic skin and decrease the influence of comorbidities associated with psoriasis. Full article

(This article belongs to the Special Issue Recent Advances in Skin Disease and Comorbidities)

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