The Role of the Skin Microbiota in Acne Pathophysiology

S. Ramasamy; E. Barnard; T.L. Dawson Jr; H. Li


The British Journal of Dermatology. 2019;181(4):691-699. 

In This Article

Human Skin Microbiota: Commensal to Harmful

A complex milieu of interactions between skin and its commensal microflora safeguards skin from day-to-day environmental influence. However, occasionally, because of imbalanced relationships, the skin commensal microbiota may shift to harmful communities in noninfectious skin-related pathologies such as atopic dermatitis, psoriasis, rosacea and acne.[19–21] This imbalance is thought to potentiate epithelial dysfunction, immune dysregulation, or overgrowth of pathogenic microbes, and may in the near future impact how we address skin pathology and disease. Gram-positive bacteria Staphylococcus epidermidis and C. acnes, and fungal species (predominately Malassezia) are the predominant residents on human epithelia and in sebaceous follicles. Present in both healthy and diseased skin, their roles as commensals or opportunistic organisms are not yet fully understood.[16,22] For example, S. epidermidis produces antimicrobial peptides, while C. acnes produces antimicrobial short-chain fatty acids, both of which function together with the host innate defence mechanisms to maintain skin health and homeostasis.[16,21] However, these microbial species are also found in opportunistic infections, especially S. epidermidis, which is a causative agent of hospital-acquired infections.[23]Malassezia are also associated with skin disease and even life-threatening septic infections.[22] Moreover, these microbes exist as interacting three-dimensional communities and biofilms, which may positively or negatively affect the skin.

One form of intramicrobial communication is robust quorum sensing and establishment of biofilms. Biofilm formation is critical in skin disease, where precise microbe–microbe network-based inputs present differential physiological signalling, rendering biofilms untreatable and antibiotic-resistant.[24–26] It has been shown that C. acnes form biofilms in follicles in some patients with acne,[27] leading to the hypothesis that an enriched presence and biofilm-based activity of C. acnes lead to homeostatic imbalance of the microbiota. It has also been speculated that the biofilm is a 'biological glue' that brings keratinocytes together to create an environment conducive to comedone development.[24,28] Unfortunately, genomic approaches alone are unable to define the presence of bacterial biofilms or the role of microbe–microbe interactions and communication. Further research using visualization techniques[29] or study of microbial interactions[30] will be necessary to understand their role and define potential interventions.

Based on our current understanding of microbiome dynamics, it will be very difficult and perhaps impossible to link the role of each microbial species with the relevant disease. Indeed, we now understand the likelihood that Koch's postulates,[31] which are based on the hypothesis of a single pathogenic species, may be impossible to meet. Koch's postulates are testable in the microbiological and cultivable sense; however, modern technological advances have complicated this interpretation because the modern methods include uncultivable microbes, and various host interaction parameters, microbial interactions and host susceptibility. Koch's postulates are also complicated by the dichotomous nature of the microbiota, shifting from commensal to opportunistic/pathogenic behaviour, including enriched and favourable expansion of cultivable single species vs. multispecies survival in the host.[16] Moving forward, it will be important to consider Koch's postulates in the light of modern data and to include the balance and imbalance of the skin microbial community in order to gain a better understanding of healthy vs. disease states.