Rosacea is a chronic cutaneous inflammatory disease that affects the facial skin. Clinically, rosacea can be categorized into papulopustular, erythematotelangiectatic, ocular, and phymatous rosacea. However, the phenotypic presentations of rosacea are more heterogeneous. Although the pathophysiology of rosacea remains to be elucidated, immunologic alterations and neurovascular dysregulation are thought to have important roles in initiating and strengthening the clinical manifestations of rosacea. In this article, we present the possible molecular mechanisms of rosacea based on recent laboratory and clinical studies. We describe the genetic predisposition for rosacea along with its associated diseases, triggering factors, and suggested management options in detail based on the underlying molecular biology. Understanding the molecular pathomechanisms of rosacea will likely aid toward better comprehending its complex pathogenesis.

Skin cancer is the most common type of cancer in the US with an increasing prevalence worldwide. While ultraviolet (UV) radiation is a well-known risk factor, there is emerging evidence that the microbiota may also contribute. In recent years, the human microbiota has become a topic of great interest, and its association with inflammatory skin diseases (i.e., atopic dermatitis, acne, rosacea) has been explored. Little is known of the role of microbiota in skin cancer, but with the recognized link between microbial dysbiosis and inflammation, and knowledge that microbiota modulates the effect of UV-induced immunosuppression, theories connecting the two have surfaced. In this paper, we provide a comprehensive review of the key literature on human microbiota, especially the skin microbiota, and skin cancer (i.e., non-melanoma skin cancer, melanoma, cutaneous T cell lymphoma). Also, mechanistic perspectives as to how our microbiota influence skin cancer development and treatment are offered.

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.

Systemic antibiotics are extensively used to control the papules and pustules of rosacea. Hence, it is crucial to understand their impact on the rosacea skin microbiota which is thought to be perturbed. The purpose of this study was to compare the makeup and diversity of the skin microbiota in rosacea before and after taking oral antibiotics. We also compared the skin microbiota at baseline according to age and rosacea severity. A longitudinal cohort study was performed on 12 rosacea patients with papules/pustules and no recent use of oral and topical antimicrobials/retinoids. Patients were prescribed oral doxycycline, 100 mg, twice daily for six weeks. Skin areas on the cheek and nose were sampled for 16S ribosomal RNA gene sequencing at baseline, and after six weeks of doxycycline treatment. Eleven females and one male aged 20–79 (median 51) with a median Investigator’s Global Assessment score of 3 (moderate) were enrolled. At baseline, Staphylococcus epidermidis was the most dominant species followed by Cutibacterium acnes (formerly Propionibacterium acnes). In the 60 Over-age group, the prevalence of Cutibacterium acnes was lower than that of the 60 & Under-age group. Rosacea severity increased with age and was associated with a decrease in the relative abundance of Cutibacterium acnes and an increase of Snodgrassella alvi. Across all subjects, antibiotic treatment reduced clinical rosacea grades and was associated with an increase in the relative abundance of Weissella confusa (P = 0.008, 95% CI 0.13% to 0.61%). Bacterial diversity (alpha diversity) was not significantly altered by antibiotics treatment. Principal coordinates analysis showed mild clustering of samples by patient (ANOSIM, Analysis of Similarity, R = 0.119, P = 0.16) and scant clustering with treatment (ANOSIM, R = 0.002; P = 0.5). In conclusion, we believe that rosacea has a unique age-dependent characteristic (i.e., severity). Although we were not able to pinpoint a causative microbiota, our study provides a glimpse into the skin microbiota in rosacea and its modulation by systemic antibiotics.

Psoriasis and psoriatic arthritis (PsA) have been recently considered as chronic systemic inflammatory disorders. Over the past decades, enormous evidence indicates that patients with psoriasis and PsA have a higher risk of developing various comorbidities including cardiovascular disease, metabolic disease, cancers, infections, autoimmune disease, and psychiatric diseases. However, reported risks of some comorbidities in those with psoriasis and PsA are somewhat different according to the research design. Moreover, pathomechanisms underlying comorbidities of those with psoriasis and PsA remain poorly elucidated. The purpose of this review is to provide the most updated comprehensive view of the risk of systemic comorbidities in those with psoriasis and PsA. Molecular mechanisms associated with the development of various comorbidities in those with psoriasis and PsA are also reviewed based on recent laboratory and clinical investigations. Identifying the risk of systemic comorbidities and its associated pathomechanisms in those with psoriasis and PsA could provide a sufficient basis to use a multi-disciplinary approach for treating patients with psoriasis and PsA.

Air pollution reportedly contributes to the development and exacerbation of atopic dermatitis (AD). However, the exact mechanism underlying this remains unclear. To examine the relationship between air pollution and AD, a clinical, histological, and genetic analysis was performed on particulate matter (PM)-exposed mice. Five-week-old BALB/c mice were randomly divided into four groups (control group, ovalbumin (OVA) group, PM group, OVA + PM group; n = 6) and treated with OVA or PM_10, alone or together. Cutaneous exposure to OVA and PM₁₀ alone resulted in a significant increase in skin severity scores, trans-epidermal water loss (TEWL) and epidermal thickness compared to the control group at Week 6. The findings were further accentuated in the OVA + PM group showing statistical significance over the OVA group. A total of 635, 501, and 2149 genes were found to be differentially expressed following OVA, PM₁₀, and OVA + PM₁₀ exposure, respectively. Strongly upregulated genes included RNASE2A, S100A9, SPRR2D, THRSP, SPRR2A1 (OVA vs. control), SPRR2D, S100A9, STFA3, CHIL1, DBP, IL1B (PM vs. control) and S100A9, SPRR2D, SPRR2B, S100A8, SPRR2A3 (OVA + PM vs. control). In comparing the groups OVA + PM with OVA, 818 genes were differentially expressed with S100A9, SPRR2B, SAA3, S100A8, SPRR2D being the most highly upregulated in the OVA + PM group. Taken together, our study demonstrates that PM₁₀ exposure induces/aggravates skin inflammation via the differential expression of genes controlling skin barrier integrity and immune response. We provide evidence on the importance of public awareness in PM-associated skin inflammation. Vigilant attention should be paid to all individuals, especially to those with AD.