Dermal photoaging refers to the skin’s response to prolonged and excessive ultraviolet (UV) exposure, resulting in inflammation, changes to the tissue, redness, swelling, and discomfort. Betanin is the primary betacyanin in red beetroot (Beta vulgaris) and has excellent antioxidant properties. Yet, the specific molecular mechanisms of betanin in HaCaT cells have not been fully clarified. The objective of this study was to investigate the activity of betanin and the underlying mechanisms in HaCaT cells; furthermore, in this study, we explored the protective effect of various concentrations of betanin against UVB irradiation on HaCaT cells. Additionally, we assessed its influence on the transcription of various epigenetic effectors, including members of the DNA methyltransferase (DNMT) and histone deacetylase (HDAC) families. Our findings demonstrate a notable downregulation of genes in HaCaT cells, exhibiting diverse patterns upon betanin intake. We considered the involvement of DNMT and HDAC genes in distinct stages of carcinogenesis and the limited exploration of the effects of daily exposure dosages. Our results indicate that betanin may protect the skin from damage caused by UV exposure. Further investigation is essential to explore these potential associations.

In recent years, artificial additives, especially synthetic food colorants, were found to demonstrate wider properties compared to their natural equivalents; however, their health impact is still not totally mapped. Our study aimed to determine the long-term (30 and 90 days) exposure effect of one of the commonly used artificial food colorants, tartrazine, on NMRI mice. The applied dose of tartrazine referred to the human equivalent dose for acceptable daily intake (ADI). Further, we evaluated its impact on the transcription of a range of epigenetic effectors, members of the DNA methyltransferase (DNMT) as well as histone deacetylase (HDAC) families. Following the exposure, organ biopsies were collected from the lungs, kidneys, liver, and spleen, and the gene expression levels were determined by real-time quantitative reverse transcription PCR (RT-qPCR). Our results demonstrated significant upregulation of genes in the tested organs in various patterns followed by the intake of tartrazine on ADI. Since DNMT and HDAC genes are involved in different steps of carcinogenesis, have roles in the development of neurological disorders and the effect of dose of everyday exposure is rarely studied, further investigation is warranted to study these possible associations.

Pemphigoid diseases are a group of chronic autoimmune blistering skin disorders, with bullous pemphigoid representing the most prevalent subtype. Bullous pemphigoid (BP) primarily affects individuals aged 60–80 years, and its incidence has been steadily rising in correlation with increasing life expectancy and population aging in Western countries. Autoantibodies targeting hemidesmosome proteins (collagen XVII and dystonin‐e) at the dermal‐epidermal junction activate complement recruiting inflammatory leukocytes that release proteolytic enzymes, degrading structural proteins and causing subepidermal blistering. The current standard treatments for pemphigoid diseases are corticosteroids and classical immunosuppressants. Systemic immunosuppression is not ideal in immunocompromised elderly patients, and more targeted and safer approaches, including dupilumab and omalizumab, are also being investigated. Our current priority is to explore further efficient and safe therapeutic options. Janus kinase (JAK) inhibitors have shown considerable potential as novel treatment options for chronic inflammatory and autoimmune diseases. The JAK inhibitors may offer efficient and safe treatment with rapid symptom improvement and disease control in the management of pemphigoid disorders. This review describes pemphigoid cases, including the rare forms, managed with JAK inhibitors (tofacitinib, baricitinib, upadacitinib, and abrocitinib).

Dermatitis herpetiformis (DH) is a chronic autoimmune blistering skin disease strongly associated with coeliac disease. This cross-sectional study investigated the clinical, serological, and neurological characteristics of 114 DH patients (70 males, 44 females; mean age: 50.2 years; 13 newly, 101 previously diagnosed) at Semmelweis University, Budapest, between 2020 and 2023. Diagnosis was confirmed by direct immunofluorescence microscopy. Serum autoantibodies against transglutaminase 2 (TG2), 3 (TG3), and 6 (TG6) were quantified using immunoassays. While at the time of evaluation, 65.8% of patients adhered to a strict gluten-free diet (GFD), 34.2% followed an incomplete or no GFD. Autoantibodies against TG2 and TG3 were each detected in 24.6% of patients, while TG6 autoantibodies were detected in 53.5%. Neurological comorbidities were reported in 43.9%, with headache and radiculopathy being the most prevalent. Hashimoto’s thyroiditis was present in 19.3%, and anaemia in 32.5% of patients. These findings, derived from a globally relevant patient cohort, underscore the systemic nature of DH and its strong association with transglutaminase autoimmunity, neurological and autoimmune comorbidities, emphasizing the need for early diagnosis, strict adherence to a GFD, and a multidisciplinary approach to optimize patient outcomes.