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Abstract

Around the beginning of the nineteenth century, Unna isolated Corynebacterium acnes (now known as Propionibacterium acnes) from acne lesions in patients, establishing the link between acne and local P. acnes infection. However, later when P. acnes was also isolated from normal, healthy skin [1], its concept as a pathogen greatly declined. In 1963, Kirschbaum and Kligman [2] re-confirmed P. acnes as a factor involved in the complex pathogenesis of acne by showing that an injection of viable P. acnes into sterile steatocystomas (as a model for sterile acne comedones) could convert these quiescent cysts into inflammatory lesions. Since then research has revealed that P. acnes influences inflammation through a wide range of pathways, ranging from neutrophil chemotaxis by P. acnes lipase [3] to direct induction of Toll-like receptors in keratinocytes [4]. However, the question remains whether this commensal is capable of initiating inflammation in the sebaceous gland and if so, why colonization does not always result in inflammation. In other words, what triggers P. acnes to play its part in acne? The answer to this question may very well be found using the concept of microbial biofilms.

Keywords

Sebaceous Gland Cystic Fibrosis Lung Neutrophil Chemotaxis Propionibacterium Acne Acne Lesion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 2014

Authors and Affiliations

  1. 1.Oystershell NVDrongenBelgium
  2. 2.Laboratory for Pharmaceutical MicrobiologyGhent UniversityGhentBelgium

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