Acne Vulgaris Research Paper
Acne Vulgaris is a disease of the epidermal pilosebaceous follicles involving inflammatory and non-inflammatory clinical lesions in the skin. The multifactorial pathogenesis of acne includes sebum, ductal epidermal hyperproliferation, colonization of Proprionibacterium acnes and inflammation . Research has shown, P. acnes is not the cause of Acne Vulgaris, but is a significant contributing factor to the inflammation stage of this disease . Sebum secretion upsurge, during times such as puberty, results in linoleic acid depletion in the follicles. This affects the barrier function of the follicular walls and as a consequence results in the influx of water from the dermis into the lumen of the follicle, which is the site of colonization of Propionibacterium
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This can then cause damage to adjacent keratinocytes and contribute to cytokine release and problematic progression of the lesions . As P. acnes causes hyperproliferation and resulting accumulation of keratinocytes, blockage in follicular duct and lumen may then ensue . This, combined with the secretion of P. acnes in biofilm establishment on the follicular walls, results in the formation of microcomedone . Cells within these biofilms exhibit altered properties,specifically pertaining to growth rate and gene transcription leading to enhanced TLR interactions . As microcomedone (primary acne lesions) progress, a wide spectrum of P. acnes products and enzymes may cause microcomedonal inflammation . Propionibacterial lipase hydrolyzes sebaceous triglycerides to produce free fatty acids . As a main metabolic acid product, propionate (Fig 1) is an irritant and contributes to the severity of the acne inflammation . Triggered by high bacterial cell density, P. acnes possess quorum sensing mechanisms through autocrine signal processes which upregulate extracellular enzyme production, such as lipase protease, hyaluronate lyase, and neuraminidase . These excretions affect both the barrier function of the follicular wall as well as keratinocyte integrity.
This can then cause damage to adjacent keratinocytes and contribute to cytokine release and problematic progression of the lesions . As P. acnes causes hyperproliferation and resulting accumulation of keratinocytes, blockage in follicular duct and lumen may then ensue . This, combined with the secretion of P. acnes in biofilm establishment on the follicular walls, results in the formation of microcomedone . Cells within these biofilms exhibit altered properties,specifically pertaining to growth rate and gene transcription leading to enhanced TLR interactions . As microcomedone (primary acne lesions) progress, a wide spectrum of P. acnes products and enzymes may cause microcomedonal inflammation . Propionibacterial lipase hydrolyzes sebaceous triglycerides to produce free fatty acids . As a main metabolic acid product, propionate (Fig 1) is an irritant and contributes to the severity of the acne inflammation . Triggered by high bacterial cell density, P. acnes possess quorum sensing mechanisms through autocrine signal processes which upregulate extracellular enzyme production, such as lipase protease, hyaluronate lyase, and neuraminidase . These excretions affect both the barrier function of the follicular wall as well as keratinocyte integrity.