The human skin is composed of a variety of key microbial genera associated with skin health, including Staphylococcus, Propionibacterium, Streptococcus, Corynebacterium and Malassezia. In particular, the Gram-positive anaerobic bacterium Propionibacterium acnes is a major resident of the normal human skin microbiota and dominates pilosebaceous units. Along with other well-described cutaneous propionibacteria (P. avidum, P. granulosum), it is believed to play an important role in maintaining skin health through ecological niches that could be colonised by more pathogenic microbes. Propionibacterium acnes produces short-chain fatty acids, thiopeptides, bacteriocins and other molecules with inhibitory properties against such organisms. P. acnes and P. granulosum are most abundant in the sebaceous gland-rich sites of the skin, which includes the face and chest.
Of the cutaneous propionibacteria, P. acnes appears the most frequent cause of opportunistic infection and is linked to a wide range of seemingly disparate conditions including the skin disease acne vulgaris.
The chronic, inflammatory and recurrent skin condition acne vulgaris is a disease of the pilosebaceous unit (hair, hair follicle, erector pili muscle and sebaceous gland) and the eighth most prevalent disease globally, affecting approximately 10% of the world’s population.
The disease has a multifactorial aetiology and is triggered initially during adrenarche in susceptible individuals and can be mild to very severe with respect to symptoms. The condition can continue, or occur for the first time, in adulthood, especially for females. Although not life-threatening, acne can have profound social and psychological effects, which are frequently more significant when symptoms are severe and scarring occurs.
It has been widely believed that the condition develops within a follicle because of four main events: androgen-induced hyperseborrhoea, follicular hypercornification, colonisation and proliferation of P. acnes, and stimulation of a local innate immune reaction.
These changes then cause a normal follicle or pore to evolve into an invisible subclinical precursor lesion known as a microcomedone, which then progresses to a non-inflammatory (open and closed comedones) and inflammatory lesion (papule, pustule or nodule). While comodogenesis was once thought to precede the inflammatory phase of lesion development, this belief has now changed with evidence that inflammation may play a fundamental role in the development of microcomedone lesions, even before keratinocyte proliferation.
Over the last decade, the development of various molecular typing methods for P. acnes, particularly multilocus sequence typing protocols validated by whole genome sequencing, has provided the opportunity to investigate the population genetic structure of the bacterium, and identify specific sequence types or lineages that may be associated with skin health and disease.
CONCLUSION
There have been significant developments in our understanding of P. acnes biology and the capacity of this bacterium to cause human disease. The observation that certain lineages are acne associated, while others appear to promote skin health, has breathed new life into the study of acne pathogenesis.
REFERENCES:
McLaughlin J, Watterson S, Layton AM, et al. Propionibacterium acnes and Acne Vulgaris: New Insights from the Integration of Population Genetic, Multi-Omic, Biochemical and Host-Microbe Studies. Microorganisms 2019:13;7:128. doi: 10.3390/microorganisms7050128.
