Abstract
The skin is the largest organ in the human and functions as a physical barrier to protect the body against foreign entities. It is also home to a vast array of microbes commonly known as the skin microbiota consisting of a variety of bacteria, fungi, and virus composition which varies between individuals and between different microenvironments of body sites. Many factors can affect the dynamic of the skin microbiota such as diets, lifestyle, or daily use of skin care products. When there is a change in the relative composition of the skin microbes compared to the homeostasis condition, the skin microbiome enters a state of dysbiosis, leading to a variety of diseases or chronic inflammatory diseases. High abundance of skin opportunistic pathogen Staphylococcus aureus (S. aureus) has been associated with the pathology of inflammatory skin diseases such as atopic dermatitis through over colonization of the skin and biofilm formation to mediate chronic infection. Skin commensal microbe Staphylococcus epidermidis (S. epidermidis) has shown to secrete antimicrobial peptides and mediate the host immune system in response to inflammation and reduce S. aureus growth during disease state. Skin care products have beneficial topical actions as well as protection against degenerative skin conditions and diseases. Natural ingredients, such as allantoin, used in skin care product preparation have gained more attention in recent years due to consumer’s increased concern about synthetic and chemical ingredients. Allantoin is an endogenous substance to the human body, resulting from the interaction of reactive oxygen species on uric acid, and is also a major metabolic intermediate in most organisms. Cutaneous bacteria such as Staphylococcal utilize uric acid as their secondary nitrogen source. Studies on functions of allantoin have shown its ability to aid in inflammatory response, also as a boost in wound healing process such as stimulation of fibroblastic proliferation and extracellular matrix synthesis. I hypothesized that allantoin treatment will increase the growth rate of skin-commensal bacteria S. epidermidis while decreasing the growth rate of the skin-pathogenic bacteria S. aureus. I also hypothesized that allantoin will increase the biofilm formation of skin commensal bacteria S. epidermidis, while decreasing the biofilm formation of skin pathogenic bacteria S. aureus. We tested allantoin effect on growth and biofilm formation of S. epidermidis and S. aureus at 0.1%, 0.5% and 1% at starting bacterial concentration of 1.0x106 CFU/mL and 1.0x108 CFU/mL. Allantoin significantly decreased S. epidermidis at both bacterial concentrations in all treatments of allantoin, while significantly increased S. aureus growth at both concentrations in all treatments of allantoin. However, allantoin significantly increased S. epidermidis biofilm formation while significantly decreased S. aureus biofilm formation at 72 hours at starting bacterial concentration of 1.0x106 CFU/mL. The results suggest that S. aureus and S. epidermidis may utilize allantoin differently in terms of growth and survival, where S. aureus utilizes allantoin for growth and S. epidermidis utilizes allantoin for biofilm formation. Future studies to investigate the mechanisms of which allantoin has an effect will provide us further information of how allantoin is affect these skin-associate microbes.