Skin microbiota: a source of disease or defence?

Abstract

Microbes found on the skin are usually regarded as pathogens, potential pathogens or innocuous symbiotic organisms. Advances in microbiology and immunology are revising our understanding of the molecular mechanisms of microbial virulence and the specific events involved in the host-microbe interaction. Current data contradict some historical classifications of cutaneous microbiota and suggest that these organisms may protect the host, defining them not as simple symbiotic microbes but rather as mutualistic. This review will summarize current information on bacterial skin flora including Staphylococcus, Corynebacterium, Propionibacterium, Streptococcus and Pseudomonas. Specifically, the review will discuss our current understanding of the cutaneous microbiota as well as shifting paradigms in the interpretation of the roles microbes play in skin health and disease.

Fig 1

Resident microflora that are beneficial to the host. The gut and mouth contain many species of microflora. Microbiota in the intestines protect the host by educating the immune system and preventing pathogenic infections. These microflora benefit the systemic immune system of the host and positively affect other organs, such as the lung. In the mouth, over 500 species of bacteria protect the mucosa from infections by preventing colonization of dangerous yeasts and other bacteria. It is yet unclear if the microflora of the skin play a similar role in protecting the host. Image from http://www.giconsults.com with permission.

Fig 2

Types of symbiotic relationships.

Fig 3

Staphylococci are pathogenic and mutualistic. (a) Virulence factors and molecules produced by staphylococci that aid in pathogenesis. (b) Staphylococci act mutually by inhibiting pathogens and priming the immune response. (c) Molecules from staphylococci that have dual functions.

Fig 4

Hypothetical model for relationship between Propionibacterium acnes and pustule formation. The graph depicts pustule formation and P. acnes growth over time. In phase 1, P. acnes is present, but comedones are not. In phase 2, comedo formation begins, independently of P. acnes growth; P. acnes begins to proliferate only after comedo forms. In phase 3, P. acnes proliferates in trapped comedo. In phase 4, P. acnes is killed by an inflammatory response. Disease and pustule formation is maximal despite eradication of P. acnes. This model illustrates that acne formation is not triggered by the ubiquitous and resident P. acnes and at the maximal disease stage, P. acnes has already been eliminated.

Fig 5

Pseudomonas aeruginosa fights fungal infections. It produces compounds such as pyocyanin, pyrrolnitrin and 1-hydroxyphenazine which kill and inhibit fungal growth. Pseudomonas aeruginosa also prevents the morphological transition of fungi from yeast-form cells to virulent filamentous cells. Filamentation of Candida albicans is associated with pathogenesis, adhesion, invasion and virulence-related products. Pseudomonas aeruginosa interacts with the host creating an environment inhospitable to fungi.