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Skin Microbiota Majalah Kedokteran Sriwijaya, Th. 52 Nomor 1, January 2020 Skin Microbiota Fifa Argentina, Rusmawardiana, Grady Garfendo Dermatology and Venereology Department, Faculty of Medicine Sriwijaya University, Palembang Email: [email protected] ABSTRACT The skin is a complex and dynamic ecosystem. It may act as physical barrier to bar the invasion of foreign pathogens while concomitantly providing home to commensals bacteria, fungi and viruses. These microbes were known as microbiota. Over a human’s life span, skin cells, immune cells, and microbiota will integrate to maintain homeostasis of skin’s physiology and immune barrier, both under healthy conditions and also under stresses (infection and wounding). Shifts in the normal microbiota may cause diseases such as atopic dermatitis and psoriasis even though pathophysiology of these conditions is still unknown. Keywords: skin microbiota, immunity 1. Introduction 2. Composition of Skin Microbiota Normal microbial flora denotes population Skin may differ commensal, non-dangerous of microorganisms that inhabit the skin and microorganisms from pathogenic mucous membranes of healthy normal skin.1 microorganisms, even though continually Skin became home to millions of bacteria, fungi exposed to them in large numbers. But this and virus that compose the skin microbiota.2 selectivity mechanism is still unclear.1 Humans have co-evolved with microbes that Assembly process of skin microbiota begins create complex, adaptive ecosystem with during birth and proceeds primarily according habitat-specific nature that are finely attuned to to body site over several weeks. Microbiota relentlessly changing host physiology.3 Skin shifts notably during puberty and adulthood. and mucous membranes harbors two groups of Despite the skin’s continuous exposure to the microorganism: (1) resident microbiota environment, microbial composition remains consists of regular microorganisms regularly stable over time. This suggests that mutually found in a given area at a given age and (2) beneficial interactions exist among commensal transient microbiota consists of non-pathogenic microbes and between microbes and the host.4 microorganism or potentially pathogenic which Several studies showed the role of microbiota resides in skin or mucous membranes for hours, in human’s health and diseases.5 days or weeks. Study showed that normal Skin is home to myriad microbial microbiota is the first line of defense against communities residing in skin surface as well as pathogen, toxin degradation and immune follicles and sebaceous glands. Skin surface has system maturation.1 Dysbiosis may cause skin varied microenvironments with different pH, diseases such as acne vulgaris, atopic temperature, humidity, sebum contents and dermatitis, psoriasis and cancer.1,3 topography.1 Skin surface is cool, acidic, and 233 Majalah Kedokteran Sriwijaya, Th. 52 Nomor 1, January 2020 bathed in sweat with only sebum and stratum 17+CD8+ T cells, which provide protection corneum peptides as well as lipids for source of against skin infections via keratinocyte nutrients. Moreover, sweat is salt-laden and induction to produce AMPs.4 consists of antibacterial molecules, such as free Fungi comprised the smallest number of fatty acids and antimicrobial peptides (AMPs). microbiotas in skin. Despite its small Nevertheless, humans and their commensal populations, fungi may have a role in microbial microbial communities have coevolved to diversification and maintain the equilibrium of provide mutual benefit.6 Studies from different microbiota community as well as host’s healtH.9 skin locations which became the usual Fungi from Malassezia genus dominated the predilections for microbial infections revealed torso and upper extremities while lower role of skin physiology as microbial community extremities were colonized by varied predictor.1 Grice et al divided bacterial skin combination of Malassezia spp., Aspergillus microbiota into 4 phyllum comprised of spp., Cryptococcus spp., Rhodotorula spp., Actinobacteria, Firmicutes, Proteobacteria and Epicoccum spp.2,9 Findley et al analyzed fungi Bacteroides. Three most common genera community of 10 adults from 14 skin sites. consist of Corynebacteria, Propinibacteria and These sites were chosen based on physiological Staphylococci.7 Each community has distinct characteristics and sites of predilection for predilections according to skin fungal-associated dermatologic diseases microenvironments. Sebaceous sites were including middle upper back, external auditory dominated by lipopHilic Propionibacterium canal, retroauricular crease, occiput, glabella, species whereas humid environments were inguinal crease, manubrium, nares, antecubital dominated by Staphylococcus and fossa, volar forearm, hypothenar palm, plantar Corynebacterium species. Less humid sites heel, toenail, and toe web (webspace between were dominated by Staphylococcus, 3rd and 4th toes). Researchers found Propinibacterium, Micrococcus, significant difference between bacterial and Corynebacterium, Enhydrobacter and fungal microbiota in human skin. Variations of Streptococcus species.1,2,8 One of the major bacterial microbiota were classified by skin genus of skin bacteria was Corynebacterium. physiology (sebaceous, humid and less humid Most of Corynebacterium species in skin did sites) and lipophilic bacteria (Corynebacterium, not cause diseases. This species’ role was Propionibacterium, Turicella) as well as shown to affect host’s health. Corynebacterium Staphylococcal species. Furthermore, fungi accolens, one of the normal skin bacteria, may microbiota was classified by skin locations inhibit the growth of Streptococcus (head, upper extremities and torso), which pneumoniae. This was in part caused by created discrete groups. Malassezia species Corynebacterial lipase that hydrolize triolein to dominated retroauricular crease, nares and oleic acid, that may inhibit pneumococcal occiput. Plantar heels were found with the most growtH.4 Other dominant group were negative- fungi variations including Malassezia, coagulase Staphylococcus species especially S. Aspergillus, Cryptococcus, Rhodotorula, epidermidis. Even though of its opportunistic Epicoccum.9 pathogen nature, S. epidermidis and S. hominis Colonization by eukaryotic DNA viruses is may secrete antimicrobial peptide which could more individually-specific. Common gene eliminate S. aureus. Studies regarding S. markers between viruses is yet to be found. This epidermidis showed evidence of skin resident means virus community diversification may bacteria’s active role in stimulating host only be detected by purified viral-like particles immunity and activating specific immune cell or shotgun metagenomics sequencing. populations. Few strains of S. epidermidis may Moreover, RNA virus can only be sequenced by induce activation of S. epidermidis-specific IL- RNA sequencing, which never be done before 234 Majalah Kedokteran Sriwijaya, Th. 52 Nomor 1, January 2020 from skin sample.2 Besides bacteriophage, inflammatory mediators release.4,6 Immune DNA virus core has yet to be found in every system evolved with resident microbiota in skin individual. Eukaryotic virus may also play a to maintain commensal equilibrium and role in skin diseases especially after the pathogen elimination. Effective discovery of Merkel cell polyomavirus, an communication between skin microbiota, oncovirus that may cause rare but aggressive epithelial cell and immune system is vital for skin cancer. Skin shotgun metagenomics may optimal mechanism. Keratinocyte may define the expansion and relative number of recognize microorganisms especially pathogen- bacterial, fungal and virus component in human associated molecular patterns (PAMPs), via skin.2,10 (Picture 1). pattern recognition receptors (PRRs). Bond between PAMPs and PRRs which triggered 3. Microbiota in Skin Immunity innate immune system (AMP), may eliminate and inactivate microorganisms including The skin has immune surveillance system bacteria, fungi and parasite.2 Skin microbial from complex combinations of epithelial cell controlled the expression of several innate tissue, lymphocyte and antigen-presenting immune factors such as AMP. Epithelial cell cells. Skin immune system may affect innate antimicrobial peptides (AMPs) derived from and adaptive immunity in stimulating immune several protein family such as cathelicidin and response. Acute skin damage releases ligand beta-defensin, and produced in keratinocyte which activate keratinocyte and triggers and sebocyte. Picture 1. Normal skin microbiota 7 235 Majalah Kedokteran Sriwijaya, Th. 52 Nomor 1, January 2020 Some of these molecules may rapidly reduce inflammation and trigger wound healing eliminate or inactivate skin pathogens such as via the ability to bind innate toll-like receptor 2 Gram positive and Gram-negative bacteria, (TLR-2) immune receptor.4 fungi, virus and parasite. Expressions of Exact mechanism of AMP, especially molecules were controlled by microbiota such induced by microbiota in microbial community as Cutibacterium species or produced by is still unclear but this relationship plays a vital certain microbes (e.g. Cutibacterium species role in skin microbial ecology. Skin microbiota peptide and AMPs by S. epidermidis).4,6 Most may control the expression level of interleukin- of Corynebacterium species in skin microbiota 1 (IL-1), cytokine involved in initiating and may not inflict diseases. Cell wall of amplifying immune response. Chain Corynebacterium consist of lipoglycan which consequences
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