Skin Microbiome

Original Editor - Oyemi Sillo

Top Contributors - Oyemi Sillo and Aminat Abolade  

This article or area is currently under construction and may only be partially complete. Please come back soon to see the finished work! (2/01/2023)

Introduction[edit | edit source]

The skin is the largest organ of the human body and it serves as a physical barrier that protects the body from invasion by foreign organisms.[1] The skin is colonized by millions of microorganisms, which make up the skin microbiome. These include bacteria, fungi, viruses, and mites. As with the gut, the microbiome of the skin plays a role in immunity, healing and health.

[2]

Composition of the Skin Microbiome[edit | edit source]

The composition of the skin microbiome varies among individuals and between body parts, and it is influenced by several factors.

Aside from host factors, interactions between microorganisms also influence the composition and function of the skin microbiome. Microbial interactions can be competitive, where the presence of one diminishes the presence of another, or synergistic, where their presence is mutually beneficial. For instance, Staphylococcus aureus colonizes the nostrils of about a third of the population and is harmless most of the time, however, it is a major risk factor for serious infection. Certain strains of Staphylococcus epidermidis have been reported to inhibit S. aureus colonization.[3]

Role of Skin Microbiome on Immunity[edit | edit source]

The skin microbiome helps to prime the cells of the immune system for response to attacks by pathogens.[1] Commensal microorganisms interact closely with the host immune cells, training T cells to respond to potential pathogen.[4] Staphylococcus epidermidis colonizes the skin during the neonatal period, possibly establishing immune tolerance by the accumulation of commensal-specific regulatory T cells following another exposure later in life.[5] Current evidence suggests that disease states are the results of microbial dysbiosis, which lead to aberrant immune responses both locally and systemically.[6] Atopic Dermatitis is an immune-mediated inflammatory disease of the skin, in which commensal bacteria of the Staphylococcus species - particularly Staphylococcus aureus - are implicated.[6]P. acnes is a commensal skin bacterium that is associated with acne, while Malassezia spp. are skin fungi that are associated with seborrhoeic dermatitis.[1]

Role of Skin Microbiome on Wound Healing[edit | edit source]

The skin microbiome has been found to play a role in wound healing. Staphylococcus epidermidis produces a secretion that reduces inflammation and speeds wound healing by binding to an immune-system receptor. There have been a lot of research into the role of the skin microbiome in the healing of chronic wounds, especially in people with diabetes. People with poorly controlled glucose levels have relatively greater abundance of Staphylococcus spp. and Streptococcus spp. Colonization. Also, studies have shown that more than half of diabetic foot ulcers are infected, with associations between the clinical features and the colonizing bacterial communities. For instance, Staphylococcus spp., particularly S. aureus, are associated with shallow ulcers and ulcers of short duration; whereas, ulcers that are deep or of long duration tend to have more diverse microbial community, with the presence of anaerobic bacteria and Gram-negative Proteobacteria spp.[3]

Physiological stressors, like metabolic disease, and psychological stressors, such as depression, can modify microbial physiology in a way that increases their virulence, causing nonpathogenic microbes to transit to a pathogenic state. This impairs the body’s wound healing responses, and promotes infections.[4] Studies on the role of microbes in wound healing have yielded contradictory results, hence there is need for more research.[7] A 2014 study found that skin wounds had accelerated and scarless healing when commensal microbes were completely absent.[8] In contrast, another study found that decrease in commensal skin bacteria following oral antibiotic use reduced wound healing rates.[9]

References[edit | edit source]

  1. 1.0 1.1 1.2 Grice, Elizabeth A, and Julia A Segre. “The skin microbiome.” Nature reviews. Microbiology vol. 9,4 (2011): 244-53. doi:10.1038/nrmicro2537
  2. nature video. The skin microbiome: a healthy bacterial balance. Available from: http://www.youtube.com/watch?v=MWE3U3FItlc [last accessed 30/12/2022]
  3. 3.0 3.1 Byrd, A., Belkaid, Y. & Segre, J. The human skin microbiome. Nat Rev Microbiol 16, 143–155 (2018). https://doi.org/10.1038/nrmicro.2017.157
  4. 4.0 4.1 Holmes, Casey J et al. “Dynamic Role of Host Stress Responses in Modulating the Cutaneous Microbiome: Implications for Wound Healing and Infection.” Advances in wound care vol. 4,1 (2015): 24-37. doi:10.1089/wound.2014.0546
  5. Nakatsuji, Teruaki, et al. “Mechanisms for Control of Skin Immune Function by the Microbiome.” Current Opinion in Immunology, Elsevier Current Trends, 16 Sept. 2021, https://www.sciencedirect.com/science/article/pii/S0952791521001199#bib0080.
  6. 6.0 6.1 Park, Young Joon, and Heung Kyu Lee. “The Role of Skin and Orogenital Microbiota in Protective Immunity and Chronic Immune-Mediated Inflammatory Disease.” Frontiers, Frontiers, 19 Dec. 2017, https://www.frontiersin.org/articles/10.3389/fimmu.2017.01955/full.
  7. Johnson, Taylor R et al. “The Cutaneous Microbiome and Wounds: New Molecular Targets to Promote Wound Healing.” International journal of molecular sciences vol. 19,9 2699. 11 Sep. 2018, doi:10.3390/ijms19092699
  8. Maria C. C. Canesso, Angélica T. Vieira, Tiago B. R. Castro, Brígida G. A. Schirmer, Daniel Cisalpino, Flaviano S. Martins, Milene A. Rachid, Jacques R. Nicoli, Mauro M. Teixeira, Lucíola S. Barcelos; Skin Wound Healing Is Accelerated and Scarless in the Absence of Commensal Microbiota. J Immunol 15 November 2014; 193 (10): 5171–5180. https://doi.org/10.4049/jimmunol.1400625
  9. Zhang, Meiling et al. “Oral antibiotic treatment induces skin microbiota dysbiosis and influences wound healing.” Microbial ecology vol. 69,2 (2015): 415-21. doi:10.1007/s00248-014-0504-4