What Lives On Our Skin: Ecology, Genomics and Therapeutic Opportunities Of the Skin Microbiome

Abstract

Our skin is home to a rich community of microorganisms. Recent advances in sequencing technology have allowed more accurate enumeration of these human-associated microbiota and investigation of their genomic content. Staphylococcus, Corynebacterium and Propionibacterium represent the dominant bacterial genera on skin and illustrate how bacteria adapt to life in this harsh environment and also provide us with unique benefits. In healthy states, our skin peacefully co-exists with commensal bacteria while fending off potentially dangerous invaders. Disruption of this equilibrium, termed "dysbiosis", can result from changes in the composition of our skin bacteria, an altered immune response to them, or both and may be a driving factor in certain types of inflammatory skin disease. Engineering topical therapeutics to favourably influence the composition of our skin flora and optimize interactions with them represents a real therapeutic opportunity for the field of dermatology and warrants additional investigation into skin microbial ecology and disease mechanisms related to host-microbe dysbiosis.

Figure 1

Skin microenvironment shapes composition of cutaneous flora: Bacteria derive nutrients from components of the stratum corneum, sebaceous, eccrine and apocrine secretions, examples of which are detailed here. Relative abundance of these skin nutrients varies by skin site and the composition of the bacterial flora fluctuates accordingly. Staphylococcus spp, which can tolerate high salt concentrations and utilize urea and amino acids in sweat as a source of nitrogen, are favored in areas with a high density of eccrine glands. By comparison, Propionibacterium spp have lipases and favor areas rich in sebaceous lipids. (AA = amino acids; FFA = free fatty acids; HCO₃⁺ = bicarbonate; H₂O = water; LHC = langerhans cell; NaCl =sodium chloride; TG = triglycerides)

Figure 2

Microbe-host dysbiosis refers to a state of imbalance with the microbiota that negatively impacts the host. This can occur primarily as a result of exogenous factors that alter the composition of the flora towards a more pro-inflammatory population. Alternatively, host susceptibility factors such as polymorphisms in innate or adaptive immune elements can lead to excess inflammation prior to any significant microbial shift. Either case can lead to a state where both the microbiota and host immune response are altered and contribute to a vicious cycle of detrimental inflammation.