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.
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.
Korean red ginseng (KRG) and ginsenosides exhibit diverse biological effects, including anti-inflammatory and anti-allergic. We aimed to investigate the therapeutic effect of KRG in a murine model of atopic dermatitis (AD) is mediated whether by diminishing the pruritus or by suppressing the inflammation. Thirty NC/Nga mice were randomly divided to 5 groups. AD-like skin lesions were induced by percutaneous challenge with 2,4,6-trinitro-1-chrolobenzene (TNCB) on the ears and backs of NC/Nga mice. KRG extract, evening primrose oil, cyclosporine, and phosphate-buffered saline were administered orally by a gastric tube. Each study group was also divided into scratching-permitted and scratching-restricted subgroups to evaluate the impact of scratching behavior on AD. The effects of KRG and the other agents were assessed by measuring the clinical severity score, ear thickness, extent of transepidermal water loss (TEWL), number of scratching movements, total systemic immunoglobulin E (IgE) and interleukin (IL)-31 levels, histologic changes of cutaneous lesions, and mRNA expression levels of tumor necrosis factor (TNF)-α, interferon (IFN)-γ, thymic stromal lymphopoietin (TSLP), and IL-31. KRG exerts therapeutic effects against AD by inhibiting the T helper 2 (Th2) mediated inflammation as well as by diminishing the itching sensation. Moreover, restricting scratching behavior suppresses the vicious cycle of itching and scratching, thus reducing clinical and systemic inflammation in our murine model of AD.
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