Clinical and pathological findings of chronic actinic dermatitis

Lin, Naiyu; Huang, Xiaobao; Ma, Chao; Han, Jun

doi:10.1111/phpp.12654

Cited by 6 publications

(16 citation statements)

References 30 publications

(53 reference statements)

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“…As well, patients are very sensitive to UV, which manifests as a relapse and aggravation of disease after a short period of UV irradiation. 24 In previous studies, we observed significant skin barrier damage in CAD patients. 25 Skin barrier damage causes external antigens to easily pass through the damaged tight junction structure.…”

Section: Discussionmentioning

confidence: 79%

LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

Wang

et al. 2022

Contact Dermatitis

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Background: Chronic actinic dermatitis (CAD) is an immune-mediated photo-allergic skin disease. In the clinic, the treatment of this disease is hampered by the lack of proper understanding of the skin barrier dysfunction mechanism.Objective: To illuminate the mechanism of skin barrier dysfunction in CAD.Methods: Transcriptome sequencing and protein profiling were used to detect skin barrier injury-related genes. RNA pull down, a promoter-reporter gene assay, and chromatin isolation by RNA purification-sequencing were used to elucidate the effect of WAKMAR2 in skin barrier functionality.Results: Transcriptome sequencing from patient's tissues showed a significantly decreased expression of WAKMAR2. Down-regulation of WAKMAR2 destroyed the keratinocyte barrier. Moreover, WAKMAR2 can directly bind to the c-Fos protein.This novel long non-coding RNA (LncRNA)-protein complexes were targeted to the CLDN1 promotor. Overexpression of WAKMAR2 enhanced the promoter activity of CLDN1, while the addition of AP-1 inhibitor could reverse this phenomenon. Furthermore, our in vivo results suggested that expression of WAKMAR2 was required for the repair of skin damage in mice induced by ultraviolet irradiation. Conclusions:We identified a crucial LncRNA (WAKMAR2) for the protection of the skin barrier in vitro and in vivo. Mechanically, it can specifically interact with c-Fos protein for the regulation of CLDN1, a finding which could be applied for CAD treatment.

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Section: Discussionmentioning

confidence: 79%

LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

Wang

et al. 2022

Contact Dermatitis

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“…UVR plays a crucial role in CAD pathogenesis, inducing both local and systematic negative effects. Furthermore, increased levels of eosinophils and total IgE are common in CAD patients, 4,12 although the precise mechanism underlying this phenomenon remains poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, increased levels of eosinophils and total IgE are common in CAD patients, 4,12 although the precise mechanism underlying this phenomenon remains poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…In severe cases, these lesions can extend throughout the whole body, accompanied by severe itching, leading to a significant deterioration in quality of life. 2 Previous studies have reported elevated levels of eosinophils and total serum immunoglobulin E (IgE) in the peripheral blood of CAD patients, [3][4][5] suggesting a close correlation with pruritus. At present, however, the underlying reasons for their elevation remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Role of interleukin‐36γ induced by ultraviolet radiation in chronic actinic dermatitis

Wang,

Tu,

et al. 2023

Photoderm Photoimm Photomed

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BackgroundChronic actinic dermatitis (CAD) is an immune‐mediated photodermatosis characterized by a high eosinophil count and total immunoglobulin E (IgE) in the peripheral blood of patients. At present, however, the reasons for their elevation remain unclear.ObjectiveThe current study aimed to detect changes in inflammatory cytokines in CAD and explore their role in this disease.MethodsEnzyme‐linked immunosorbent assay and Luminex assay were conducted to measure inflammatory factor levels. Immunohistochemical analysis and quantitative real‐time polymerase chain reaction were performed to evaluate the expression levels of interleukin‐36γ (IL‐36γ), IL‐8, chemokine (C‐C motif) ligand 17 (CCL17), and CCL18. CCK8 kits were used to assess cell proliferation. Immunofluorescence was used to detect nuclear factor κB (NF‐κB) p65 nuclear translocation. Western blot analysis was performed to detect the protein expression level of phosphorylated NF‐κB (p‐NF‐κB) p65. Hematoxylin and eosin and Masson trichrome staining were applied to observe histological changes in a chronic photo‐damaged mouse model.ResultsEosinophils, total IgE, IL‐36γ, IL‐8, tumor necrosis factor α, CCL17, and CCL18 were elevated in CAD. Of note, IL‐36γ promoted the proliferation of eosinophilic cells (EOL‐1) and the production of IgE in peripheral blood mononuclear cells. IL‐36γ also promoted the production of IL‐8 and CCL18 in immortalized human keratinocytes (HaCaT cells), while ultraviolet radiation (UVR)‐induced IL‐36γ via activation of the NF‐κB signaling pathway.ConclusionsIL‐36γ was involved in the pathogenesis of CAD and UVR contributed to the production of IL‐36γ, which may provide a novel therapeutic target for CAD.

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“…CAD is an immune-mediated photodermatosis. As the disease progresses, the lesioned skin becomes rough and thickened, with mossy lesions and increased pruritus, and patients may even scratch the skin and suffer complications such as local skin infections and artificial dermatitis [15,16].…”

Section: Discussionmentioning

confidence: 99%

Curcumin Improves Keratinocyte Proliferation, Inflammation, and Oxidative Stress through Mediating the SPAG5/FOXM1 Axis in an In Vitro Model of Actinic Dermatitis by Ultraviolet

et al. 2022

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Background. Chronic actinic dermatitis (CAD) is an abnormally proliferating photoallergic skin disease. Dysregulated inflammation and oxidative stress are the immediate factors in the abnormal proliferation of keratinocytes. This study aimed to investigate the effect of curcumin on the aberrant proliferation of keratinocytes in an in vitro (actinic dermatitis) AD model and the possible molecular mechanisms. Methods. The keratinocytes were irradiated with ultraviolet (UV) to construct an in vitro AD model and then processed with different concentrations of curcumin. Cell viability, oxidative stress markers (SOD, GSH-PX, and MDA), activated oxygen species (ROS), and inflammation markers (IL-1β, IL-6, IL-18, and TNFα) were determined, respectively. Western blot was applied to assay the profiles of apoptosis-related proteins (Bax, Bcl-xL, Caspase3, Caspase8, and Caspase9), oxidative stress proteins (Keap1, Nrf2, HO-1, COX2, and iNOS), and inflammatory proteins (NF-κB, MMP1, and MMP9) and SPAG5/FOXM1. Functionally, SPAG5 or FOXM1 overexpression and knockdown models were constructed in keratinocytes to characterize their influence on UV irradiation-mediated keratinocyte dysfunction. Results. Curcumin weakened UV-mediated inflammation, proliferation, and oxidative stress and impaired apoptosis in keratinocytes. UV boosted SPAG5/FOXM1 expression in cells, while curcumin concentration-dependently retarded SPAG5/FOXM1 expression. Overexpression of SPAG5/FOXM1 fostered UV-mediated inflammation, proliferation, oxidative stress, and intensified apoptosis, whereas curcumin mostly reversed the SPAG5/FOXM1-mediated effects. In addition, knocking down SPAG5/FOXM1 ameliorated UV-mediated keratinocyte dysfunction, whereas curcumin failed to exert further protective effects in cells with knockdown of SPAG5/FOXM1. Conclusion. Curcumin modulated proliferation, inflammation, oxidative stress, and apoptosis of keratinocytes by restraining the SPAG5/FOXM1 axis.

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Clinical and pathological findings of chronic actinic dermatitis

Cited by 6 publications

References 30 publications

LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

Role of interleukin‐36γ induced by ultraviolet radiation in chronic actinic dermatitis

Curcumin Improves Keratinocyte Proliferation, Inflammation, and Oxidative Stress through Mediating the SPAG5/FOXM1 Axis in an In Vitro Model of Actinic Dermatitis by Ultraviolet

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