The skin barrier, composed of lipids and essentially dead cells (corneocytes) in the upper layer of the epidermis (stratum corneum), plays a major role in protecting the body from numerous insults including microbial invasion. However, when compromised, the skin’s immune system is activated to defend the body from further damage and infection. Skin immunity involves the skin microbiome (collective set of microorganisms on the skin), antimicrobial peptides (short chains of amino acids) and a variety of signaling molecules that activate or suppress certain immune cells such as dendritic cells (including Langerhan’s cells), macrophages, neutrophils and mast cells.
When damage and/or infection is detected, a response known as inflammation typically occurs. Viniferamine® skin and wound care products like Renewal Moisturizer include ingredients that sooth skin and inflammation-associated irritation that can lead to skin breakdown. Many of the small molecule ingredients found in Viniferamine® skin and wound care products have potent anti-inflammatory activities including the small molecule polyphenols oleuropein, resveratrol, and epigallocatechin-3-gallate (EGCG) from olives, grapes, and green tea, respectively, as well as the important small molecules, melatonin, and L-glutathione. In addition, dipotassium glycyrrhizate from licorice, avenanthramides in oats, aloe vera and shea butter possess anti-inflammatory activities.
The skin microbiome communicates with the skin’s immune system and affects inflammatory responses. A common microbe found on skin, Staphylococcus epidermis (S. epidermis), has been shown to modify inflammatory responses and influences immune cell recruitment. Evidence indicates that S. epidermis can stimulate the expression of antimicrobial peptides that are able to inhibit invading Staphylococcus aureus (S. aureus). In the epidermis, keratinocytes (cells that become corneocytes) produce antimicrobial peptides in response to infection including human beta-defensins and cathelicidins (CAMPs) that are found in the stratum corneum.
Studies have shown that CAMP expression increases following wounding, oxidative stress, and epidermal barrier disruption. The lipid, ceramide, generated during epidermal stress also stimulates CAMP production. Ceramide improves the epidermal barrier and its production is stimulated by niacinamide found in Viniferamine® skin and wound care products. In addition, a recent study found that resveratrol (from grapes) stimulates CAMP production and it has been shown that vitamin D (from oat extract in Viniferamine® products) stimulates CAMP.
Other vitamins found in Viniferamine® products including Silicone Barrier stimulate skin immunity such as vitamin C (ascorbic acid), which has been shown to prevent typical decreases in Langerhan’s cell numbers that occur following UV radiation. Vitamin C is also thought to support skin neutrophil functions such as bacterial killing as well as skin macrophage clearing of dead cells. Vitamin C and vitamin D also promote wound healing, which requires proper inflammatory and other immune responses stimulated by these important vitamins.
Many ingredients in Viniferamine® skin and wound care products promote wound healing including oleuropein that was shown to improve wound healing in an aging model. Resveratrol has been shown to improve wound healing in individuals with type 2 diabetes. EGCG has been shown to accelerate keratinocyte differentiation and wound healing, and melatonin was shown to accelerate the process of wound repair in full-thickness incisional wounds. In addition, L-carnosine stimulated wound healing in an incision wound model and L-glutathione was beneficial for ischemic wound healing. Moreover, Centella asiatica and one of its main components, asiaticoside have important wound healing activities, and dipotassium glycyrrhizate is known to protect hyaluronic acid, which plays an important role in wound healing.
Several studies also indicate that the olive polyphenol, oleuropein can regulate immune cells including macrophages, neutrophils and mast cells. Oleuropein has been shown to either stimulate or suppress inflammatory responses of macrophages depending on the conditions and cell environment. In fact, oleuropein has been found to inhibit mast cell and neutrophil degranulation to help regulate inflammation. In addition, an important molecule found in aloe vera, acemannan has been shown to upregulate macrophage killing and engulfment of Candida albicans, a common cause of skin yeast infections.
It’s good to know that Viniferamine® skin and wound care products like Renewal Moisturizer and Silicone Barrier include ingredients that help regulate inflammation and stimulate immune responses against skin pathogens. In addition, Viniferamine® products preserve the natural chemistry and pH of skin to protect the skin microbiome that also stimulates skin immunity.
About the author: Nancy Ray, PhD is the Science Officer at McCord Research. Dr. Ray received her PhD in Biochemistry and Biophysics and was a postdoctoral fellow at NIH, Harvard University and Dana-Farber Cancer Institute, and the University of Iowa. She also earned bachelor of science degrees in Chemistry and Microbiology.
- J Clin Exp Dermatol Res 2012; S2:003.doi:10.4172/2155-9554.S2-003:1-6.
- Arch Immunol Ther Exp 2018; 66: 45-54.
- Int J Mol Sci 2014; 15: 18508-18524.
- Diab Vasc Dis Res 2014; 11: 92-102.
- Oxid Med Cell Longev 2012; ID 560682:1-8.
- J Pineal Res 2013; 55: 325-356.
- Int J Gen Med 2011; 4: 105-113.
- Evid Based Complement Altern Med 2012; ID 650514:1-9.
- Cell J 2014; 16: 25-30.
- ISRN Endicronol 2014; ID 816307: 1-8.
- J Am Acad Dermatol 2005; 52: 1049-1059.
- Br J Dermatol 2014; 171: 19-28.
- J Invest Dermatol 2013; 133: 1942-1949.
- J Clin Aesthet Dermatol 2017; 10: 14-17.
- Nutrients 2017; 9: 866; doi:10.3390/nu9080866: 1-27.
- J Adv Res 2015; 6: 793-804.
- J Pineal Res 2008;44: 387-396.
- Surgery 1986;100: 815-821.
- Ann Plast Surg 2007;58: 449-455.
- BMC Complement Altern Med 2012;12: 1-7.
- Phytother Res 1999;13: 50-54.
- Cosmet Toilet 2010;125: 1-9.
- Wound Repair Regen 1999;7: 79-89.
- Life Sci 1998; 62: 541-546.
- J Agric Food Chem 2015; 63: 2098-2105.
- Inflammopharmacol 2017; 25: 673-680.
- Phytomed 2014; 21: 1400-1405.
- Int J Immunopharmac 1997; 19: 75-82.
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