Main trigger of acne vulgaris has been known to involve P. acnes, and antimicrobial agents have been commonly used in Europe and the US for treatment. Kistowsca and Qin reported on the activation of inflammasome and TLR 2, caused by P. acnes. Thiboutot, however, raised the question as to how P. acnes interacts with immune cells at the initial stage of acne lesions, when no P. acnes is present in the cutis, which epidermis is intact and has no follicular wall rupture. Meanwhile, the evidence of inflammatory cytokines such as IL-1β is reported in the initial stage of the lesions. In this research, we conducted an analysis of the contents of comedones in order to find a possibility of a causative factor other than P. acnes with which the expression of inflammatory cytokines and activation of NLRP 3 inflammasome may occur. We extracted the contents of comedones with 70% ethanol and analyzed them by using a method with a liquid chromatography mass spectrometry. Many lipid mediators and lipid peroxide including arachidonic acid metabolite were detected in the analysis. Some differences in lipid mediators and lipid peroxide among comedones were also detected. By comparing the inflammatory and non-inflammatory lesion comedones, namely according to the classical nomenclature classification, our findings suggest there may be a factor other than P. acnes that may contribute to the pathophysiological mechanism of acne vulgaris and the activation of NLRP 3 inflammasome.

The analysis of comedones in acne vulgaris by using a method with a liquid chromatography mass spectrometry.