Журнал клинических и экспериментальных дерматологических исследований
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ISSN: 2155-9554
ISSN: 2155-9554
Anthony Linfante, Rina M. Allawh and Herbert B. Allen
Acne vulgaris is traditionally known as the result of excess sebum production, follicular hyper keratinization, infection with Propionibacterium acnes, and follicular inflammation. However, the role of P. acnes is gaining momentum as the primary impetus in the pathogenesis of acne vulgaris. The biofilm-forming ability of P. acnes in vitro and on indwelling medical appliances and catheters has been known for quite some time, but only in the last decade has the presence of P. acnes biofilm been observed within the pilosebaceous unit. Since that time, the genome of the microbe has been sequenced, and genes responsible for quorum sensing and biofilm formation have been confirmed. As a result of biofilm formation, the virulence of P. acnes is amplified. Biofilm-encapsulated P. acnes upregulates the production of lipases, resulting in the production of free fatty acids. Free fatty acids as well as the biofilm itself bind the Toll-like receptors TLR2 and TLR4, activating the innate immune system, culminating in a robust inflammatory response. Biofilms also appear to significantly contribute to antibiotic resistance. Acting as a physical barrier for antibiotics as well as a commune for bacteria to exchange antibiotic resistance genes, the biofilm plays an integral role as the major hurdle to treating acne vulgaris. Traditional antimicrobials have not shown much promise in disruption of the biofilm. Other approaches have been investigated utilizing a variety of novel topical compounds that act to prevent or disrupt the biofilm as a therapeutic modality. The role of biofilm in the pathogenesis of acne vulgaris has remained underappreciated, but with global antimicrobial resistance looming, further attention may be warranted