Skin Microbiome: An Actor in the Pathogenesis of Psoriasis

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INTRODUCTIONPsoriasis is characterized by raised, scaly, well-demarcated, erythematous oval plaques.[1] Although studies have revealed that disruption of immune tolerance and excessive production of inflammatory factors play important roles in the pathogenesis of psoriasis, the exact mechanism is still not clear.[2] Previous studies have shown that the concordance rate of monozygotic twins with psoriasis is greater than that of dizygotic twins,[34] with genetic factors underpinning 66–90% of the variation in risk of developing psoriasis.[5] These studies reveal not only the genetic influence on psoriasis but also that nongenetic factors are important in the pathogenesis of psoriasis.Each one of us is colonized by some 100 trillion bacteria that reside in our intestines, mouth, nose, genitals, and skin.[6] As a critical barrier to the outside world, human skin is the body's largest and most exposed organ. Human skin closely interacts with the exterior environment, and the commensal microbiota at the skin play an important role in maintaining the function of skin barrier.[6] An assemblage of microorganisms, including bacteria, fungi, viruses, and arthropods, colonize the human skin and together form the skin microbiome.[7] The skin microbiome plays an important role in maintaining human health through inhibition of invasion by pathogens, formation of biofilms, and production of antibacterial peptides. Recent studies indicate that the composition of the human skin microbiome is closely related to many diseases including atopic dermatitis,[8] psoriasis,[9] and acne vulgaris.[10] In this review, we will focus on the relationship between the skin microbiome and the function of the skin barrier, the microbiome changes in psoriasis, and the possible pathogenic mechanisms involved.SKIN MICROBIOME AND THE SKIN BARRIERBecause skin is protective against physical, biological, and chemical stress, it is considered to be an effective barrier between the body and the environment.[11] The skin consists of epidermis, dermis, and hypodermis. Epidermis is stratified into four layers according to the stage of keratinocyte differentiation: stratum corneum, stratum granulosum, stratum spinosum, and stratum basale.[12] The skin barrier is formed by differentiating keratinocytes and is continuously renewed. Previous studies have showed that the stratum corneum and epidermal tight junctions are two of the main elements in the barrier function of the skin.[13] The microbial ecology of human skin is complex and may play an important role in diseases. Studies focusing on healthy volunteers have demonstrated that Staphylococcus, Micrococcus, Corynebacterium, Brevibacteria, Propionibacteria, and Acinetobacter species regularly reside in normal skin.[14] The most common fungal species present on normal human skin are Malassezia.[15] A study of 11 body locations (the forehead, left and right axillae, left and right inner elbows, left and right forearms, left and right forelegs, and behind the left and right ears) from eight healthy adult participants showed that Malassezia accounts for up to 80% of the fungi on the skin.[16] Both environmental and host factors can affect the skin microbiome such as climate, body location, age, and gender.[17] For site-specific composition, the skin microbiome was found to be quite different across the population. However, when skin sites with bilateral symmetry were compared, the intraindividual variability of the skin microbiota had a high level of conservation.[1418]Staphylococcus has been associated with impaired wound healing in both clinical and laboratory models. Mullikin et al. found that a longitudinal selective shift of microbiota coincided with aberrant expression of innate immunity genes in diabetic mice. Moreover, they detected aberrant expression of innate immunity genes associated with the significantly enriched cutaneous host defense response and increased Staphylococcus abundance.[19] Zeeuwen et al.

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