Mark V. Dahl, MD

P. acnes activates the inflammasome in human sebaceous glands.

Propionibacterium acnes plays a role in the inflammatory papules of acne vulgaris, perhaps initiated by inflammasomes. The innate immune system senses bacterial invasion through recognition of pathogen-associated molecular patterns (PAMPs) and host-derived signals (damage-associated molecular patterns, or DAMPs). Recognition initiates assembly of large complexes called inflammasomes, which activate caspase-1, leading to release of the proinflammatory cytokines interleukin-1β (IL-1β) and interleukin-18.

These authors found more IL-1β expression in acne papules than in healthy skin, and expression was especially prevalent in macrophages surrounding pilosebaceous units. In cultured human sebocytes, they found mRNA for most components of inflammasomes. Exposing sebocytes to P. acnes upregulated cytoplasmic expression, release, and activation of IL-1β. Activation of the inflammasome called NLRP3 was dependent upon metalloprotease activity. Caspase-1 was also activated. When NLRP3 expression was inhibited, P. acnes-induced IL-1β production was extinguished in sebocytes. Mice deficient in NALP-3, another inflammasome, showed reduced inflammation after intradermal injection of live P. acnes. Thus, it appears that human sebocytes contain the necessary elements to form inflammasomes.

Citation(s):

Li ZJ et al. Proprionobacterium acnes activates the NLRP3 inflammasome in human sebocytes. J Invest Dermatol 2014 Nov; 134:2747.