Acne sans P. acnes

Abstract

Acne vulgaris is a common disease that carries an enormous financial and psychosocial impact. Androgens, excessive sebum production, ductal hypercornification, changes in the microbial flora, as well as inflammation and immunological host reactions are considered the major contributors to acne pathogenesis. Despite extensive research on acne pathogenesis, the exact sequence of events and their possible mechanisms leading to the development of a microcomedone and its transformation into an inflamed lesion has remained unclear. There is a significant amount of in vitro evidence suggesting a possible pathogenetic role for Propionibacterium acnes in comedogenesis as well as inflammation in inflammatory acne. However, the microbiological data from non‐inflamed as well as inflamed acne lesions, cultured individually, do not entirely support the hypothesis that these micro‐organisms are actually responsible for their initiation. There appears to be comedones and inflamed lesions in which there is no clear evidence of Propionibacterium acnes involvement. Considering this microbiological data, alongside the in vitro evidence, we have tried to delineate the possible sequence of events and their mechanisms, leading to the development of a microcomedone and its transformation into an inflamed lesion. Based on the available literature we have analysed the evidence of both non‐inflamed as well as inflamed acne lesions occurring in the absence of Propionibacterium acnes from the pilosebaceous follicles. We propose that the development of an inflamed acne lesion depends on an imbalance between the pro‐inflammatory and anti‐inflammatory pathways rather than the incitement of inflammation by Propionibacterium acnes.

Acne

“…Initiation of acne likely does not require P. acnes , as shown by the fact that propionibacteria are not always isolated from acne lesions [ 17 ] . However, propionibacteria contribute to disease aggravation by secreting infl ammation-promoting metabolites such as lipases, which release (irritant) free fatty acids from triglycerides, as well as proteases, hyaluronidases, and chemotactic factors.…”

A Derivative of the Thiopeptide GE2270A Highly Selective against Propionibacterium acnes

“…Buffers used were the following: buffer A, 25 mM Tris-HCl (pH 7.1), 5% glycerol, 700 mM NaCl, 6 mM ␤-mercaptoethanol, 0.1 mM phenylmethylsulfonyl fluoride (PMSF), 0.1 mM benzamidine; buffer B, 25 mM Tris-HCl (pH 7.1), 300 mM NaCl, 5% glycerol, 20 mM imidazole, 6 mM ␤-mercaptoethanol, 0.1 mM PMSF, and 0.1 mM benzamidine; buffer C, 25 mM Tris-HCl (pH 7.1), 300 mM NaCl, 5% glycerol, 300 mM imidazole, 6 mM ␤-mercaptoethanol, 0.1 mM PMSF, 0.1 mM benzamidine; buffer D, 20 mM Tris-HCl (pH 7.1), 100 mM NH 4 Cl, 5% glycerol, 6 mM ␤-mercaptoethanol, 0.1 mM EDTA; buffer E, 10 mM Tris-HCl (pH 7.7), 10 mM magnesium acetate, 60 mM NH 4 Cl.…”

“…The organism catabolizes sebaceous triglycerides, using the glycerol moiety as a carbon source without catabolizing the fatty acids. While this species has been advocated to play a fundamental role in the etiogenesis of acne (5,6), a significant controversy remains as to how important a role P. acnes plays (4,7). Recent metagenomic studies have confirmed it to be the major inhabitant of pilosebaceous units (8).…”

“…Although it affects almost 100% of adolescents to various degrees and generally wanes as adolescence ends, the disease may persist into adulthood, and it has been estimated that more than 17 million people in the United States are affected by acne (1,2). At least four factors contribute to the development of acne: increased sebum production by the sebaceous glands, follicular hyperkeratinization, colonization of the sebaceous follicles with Propionibacterium acnes, and inflammation (3,4).…”

Tobacco Smoke and Chloracne: An Old Story Comes to Light

“…There are various forms of acne, and so different sequences of events are likely. A severe form of acne, known as ‘chloracne' and leading to the formation of metabolising acquired dioxin-induced skin hamartoma (MADISH) [3,4], is clearly associated with the exposure of chemicals such as polychlorinated dibenzodioxins and dibenzofurans [5,6,7], and does not require the presence of Propionibacterium acnes [8]. The main feature of these chemicals is the activation of aromatic hydrocarbon receptor (AhR).…”