| dc.description.abstract | A vibrant range of microbiome has been annexed in the skin that are proficient in extracellular electron transfer (EET) and beyond innately engaged in different molecular tasks. Ultraviolet-B (UV-B) radiation was indeed known to trigger deeper tissue shift as well as to attenuate the immune reaction. The importance of the microbiome was hardly debated in UV-induced skin insults. Bacteria have been using electron transport proteins throughout the membrane to generate electricity in the intestinal microbiome that has been identified recently. Although, the characterization of electrogenic bacteria in the skin microbiome seems to be almost completely unmapped. We have outlined the skin Staphylococcus epidermidis (S. epidermidis) as an electrogenic bacterial strain using a ferric-ferrozine investigation. The fermentation of glycerol is vital for the production of electricity in S. epidermidis while inhibition of 5-methyl furfural (5-MF) significantly reduced the bacterial electricity measured in a fuel cell by voltage changes (MFC). In order to investigate the impact of UV-B on electricity generation and UV-B bacterial resistance in S. epidermidis bacteria, a small-scale chamber with both anode and cathode was developed. Though UV-B decreased bacterial electricity, prolonged glycerol incubation led to fermentation of S. epidermidis and increased electricity to counteract UV-B effect. Electricity produced by human skin-based bacteria may be used as an adaptive biomarker to depict ultraviolet radiation in live time.
The exploration of skin prebiotics for skin probiotics have not been well defined and may be instigated by retrofitting existing skincare compounds for new indications. Four compounds that have been registered by the International Nomenclature of Cosmetic Ingredients (INCI) were included to study their abilities to induce the fermentation of Staphylococcus epidermidis (S. epidermidis), a bacterial species abundant in the human skin. Liquid coco-caprylate/caprate (LCC), originally used as an emollient, effectively initiated the fermentation of S. epidermidis, produced short-chain fatty acids (SCFAs), and provoked robust electricity. Application of LCC plus S. epidermidis on mouse skin significantly reduced ultraviolet B (UV-B)-induced injuries which were evaluated by the formation of 4-hydroxynonenal (4-HNE), cyclobutane pyrimidine dimers (CPD), and skin lesions. An S. epidermidis S2 isolate with low expressions of genes encoding pyruvate dehydrogenase (pdh), and phosphate acetyltransferase (pta) was found to be poorly electrogenic. The protective action of S. epidermidis plus LCC against UV-B-induced skin injuries was considerably suppressed when mouse skin was applied with LCC in combination with the S. epidermidis S2 isolate. Exploring new indication of LCC for promoting S. epidermidis against UV-B provided an example of repurposing INCI-registered compounds as skin prebiotics.
The host may benefit from the prevalent bacteria present in the skin microbiome. Topical application of S. epidermidis plus glycerol onto mouse skin mitigated the UV-B-induced production of labile ferrous ion (Fe2+), 4-HNE (4-hydroxy-2-nonenal), and cyclobutene pyrimidine dimers (CPD), demonstrating that bacterial electricity acts to attenuate oxidative damage caused by UV-B. The regulation of gene expression of Type II NADH hydrogenase gene (ndh2) and production of demethylmenaquinone-8 (DMK-8) in EET systems for the production of electricity was critical in Cyclophilin A present in S. epidermidis. Suppression of cyclophilin A axed electron generation and considerably reduced the anti-UV activity of S. epidermidis fermentation. Cumulatively, we demonstrate for the first time that electrogenic skin bacteria facilitate a cyclophilin A-mediated pathway to generate electricity as a defense against UV. | en_US |