Bacterial hypercolonization of the sebaceous follicle, especially with Propionibacterium acnes, has been considered as a major causative factor for acne vulgaris [1, 2]. In addition, it is widely accepted that inflammation in acne may be mainly mediated by an immunological reaction to extracellular products of P. acnes, such as sebum free fatty acids which are proposed to be products of triglyceride metabolism induced by follicular bacteria [1–3]. However, it is by no means clear that either bacteria or their products initiate follicular inflammation. P. acnes is found both in acne and normal pilosebaceous units [4]; therefore, its role in acne cannot be explained by its presence in the follicle. In addition, the number of follicular bacteria on untreated skin of acne patients does not correlate with the grade of severity of acne [1]; high numbers of follicular bacteria have also been found in individuals without acne.
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Christos C. Zouboulis (2001) studied this question.
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