Background Systemic antioxidants, such as oral Polypodium leucotomos extract (PLE), have been found to have photoprotective properties. Objective This study was designed to objectively evaluate the molecular and photobiologic effects of oral administration of PLE. Methods 22 subjects with Fitzpatrick skin phototype I–III were enrolled. On day 1, subjects were irradiated with visible light, ultraviolet A1 (UVA1) and ultraviolet B (UVB; using 308-nm excimer laser). Evaluation was done immediately and 24 hours after irradiation. On days 3 and 4, irradiation and evaluation process was repeated after ingestion of PLE. Results Clinical assessments and colorimetry data showed a decrease in UVB -induced changes in 17 out of 22 subjects post-PLE administration; histology findings demonstrated such a decrease in all 22 subjects. Limitations Only 2 doses of PLE were given. Furthermore, subjects with skin phototypes I–III only were studied. Conclusion This is the first demonstration that PLE has objective measurable suppressive effects on UVB-induced erythema within 2 hours of administration. The results suggest that PLE can potentially be utilized as an adjunctive therapy to lessen the negative photobiologic effects of UVB. In addition, this is the first study to demonstrate the potential correlation between non-invasive colorimetry outcomes and UVB induced molecular damage.

Summary Background Actinic keratoses (AKs) are common premalignant skin lesions triggered by excessive ultraviolet exposure. The majority of AKs regress or persist, but some progress to squamous cell carcinomas. Biomarkers associated with their persistence, progression and regression have not been characterized. Objectives We performed skin biopsies in patients with extensive actinic damage to identify biomarkers that correlate with clinical progression and regression of AKs. Methods This was an observational study of a cohort of patients with extensive actinic damage. AKs were mapped on a clear plastic template in 26 patients at months 3, 6, 9 and 11. Biopsies were taken from randomly selected, predetermined AKs and were evaluated for p53, E‐cadherin, Snail, Slug and Twist. The study is registered at Clinicaltrials.gov: NCT00027976. Results p53 exhibited greater expression in clinically apparent AKs (histological score 2·89 ± 1·45) than in regressed AKs (0·75 ± 0·96); P < 0·01. There was also significantly less membrane E‐cadherin, the lack of which is a marker of epithelial–mesenchymal transition, in clinically apparent AKs (1·89 ± 1·81) than in sun‐exposed skin (3·07 ± 1·75); P < 0·005. The E‐cadherin transcription repressors Snail, Slug and Twist were increased in AKs compared with sun‐exposed skin. A limitation of the study is that measurement of histological biomarkers was not a primary end point. In addition, patients were allowed to apply sunscreens. Conclusions At the molecular level, loss of E‐cadherin and an increase in p53 are linked to the dynamic interplay between the persistence, progression and regression of AKs. What's already known about this topic? Actinic keratoses (AKs) are common dysplastic epidermal lesions that result from chronic and excessive ultraviolet exposure. Biomarkers associated with progression and regression of AK have not been characterized. What does this study add? Decreased E‐cadherin and increased p53, Snail, Slug and Twist (E‐cadherin transcription factors) were associated with progression from AK to nonmelanoma skin cancer. What is the translational message? Strategies targeting these molecules may be effective in reversing rising skin cancer rates. E‐cadherin, p53, Snail, Slug and Twist are potential biomarkers that may be used to assess the efficacy of existing chemopreventive agents.

SummaryThe saliva proteome includes host defense factors and specific bacterial-binding proteins that modulate microbial growth and colonization of tooth surface in the oral cavity. A multidimensional mass spectrometry approach identified the major host-derived salivary proteins which interacted with Streptococcus mutans (strain UA159), the primary microorganism associated with the pathogenesis of dental caries. Two abundant host proteins were found to tightly bind to S. mutans cells, common salivary protein-1 (CSP-1) and deleted in malignant brain tumor 1 (DMBT1, also known as salivary agglutinin or gp340). In contrast to gp340, limited functional information is available on CSP-1. The sequence of CSP-1 shares 38.1% similarity with rat CSP-1. Recombinant CSP-1 (rCSP-1) protein did not cause aggregation of S. mutans cells and was devoid of any significant biocidal activity (2.5 to 10 μg/ml). However, S. mutans cells exposed to rCSP-1 (10 μg/ml) in saliva displayed enhanced adherence to experimental salivary pellicle and to glucans in the pellicle formed on hydroxyapatite surfaces. Thus, our data demonstrate that the host salivary protein CSP-1 binds to S. mutans cells and may influence the initial colonization of this pathogenic bacterium onto tooth surface.

Drs Oak and Shafi contributed equally to the manuscript.Funding sources: California Table Grape Commission.IRB approval status: Reviewed and approved by the University of Alabama at Birmingham IRB; approval #F140627004.