The Skin Microbiome: Is There a Role in the Pathogenesis of Atopic Dermatitis and Psoriasis?

The secondary pool of genomic information provided by bacteria, fungi, viruses and other microorganisms that constitute the totality of an organism’s resident microbial community create what clinicians and investigators now refer to as a “microbiome.”^1,2 The advent of microbiome studies via the utility of high throughput genomic sequencing has uncovered a revolutionary perspective regarding the investigation of disease pathogenesis—rather than focusing on invading pathogens as the sole etiological agents of certain diseases, shifts in an individual’s microbial community profile are now being evaluated as associated culprits in disease causation. Thus, appreciation of the unique interaction between inhabitant microbial flora, the host’s endogenous genetic factors and exogenous environmental elements reveal that maintenance of this complex symbiotic relationship between human host and resident microbes is essential for facilitating tissue homeostasis. Of particular interest, studies have associated alterations in the hyperdiverse microbial communities that colonize human skin with the pathogenesis of commonly diagnosed dermatological diseases.^3-5 This mini-review will survey and summarize some of the recent studies conducted with similar high throughput technologies that suggest modifications in the ecology of skin microorganisms play a critical role in the disease process for atopic dermatitis and psoriasis.

The human microbiome is invariably established shortly after birth due to the rapid colonization of microorganisms that outnumber host cells 10-fold.⁶ The resulting microbial ecosystem exhibits stable resident populations, found endogenously and superficially, as well as transient populations.⁷ The total composition of resident commensal organisms is contingent upon key biological factors including temperature, sebum content, antibiotic/probiotic use, humidity, and pH.^8,9 Skin possesses the ability to shape the aggregate microbiome by facilitating the colonization of commensal organisms while effectively warding off pathogenic organisms through mechanisms like desquamation and the release of inducible and constitutively expressed antimicrobial peptides.¹⁰ For years, microbial dysbiosis has been recognized as a way for typically benign residential organisms to convert into pathogenic agents.^6,11 The harsh, desiccated environment of the skin also acts to inhibit the proliferation of pathogenic invaders of the skin.¹⁰

Rather than characterizing skin microflora as a monolithic entity, skin microbiome studies have elucidated the understanding that distinct anatomical locations harbor unique populations of microorganisms that function in both health and disease states.^1,2,8 Furthermore, differing concentration of adnexal structures such as hair follicles, sebaceous, eccrine, and apocrine glands may very well contribute to the microbiome’s phylogenetic hyperdiversity.¹² Traditional methods of culturing that often identified Staphylococcus, Corynebacterium, Propionibacterium, Streptococcus and Pseudomonas as key constituents of skin microbiota have been expounded upon with the standardization of 16S rRNA gene sequencing.^8,9 Evidence now suggests that human skin includes upwards of 100 phylotypes that belong to 6 divisions of bacteria.^10,13 Regions of