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MEN’S GROOMING 25


variants, i.e. phylotypes, some of which can be considered to be ‘neutral’ and some as virulent (‘aggressive’). The ‘neutral’ phylotypes of C. acnes normally dominate the hair follicles, whereas the virulent phylotypes only dominate the hair follicle in acne lesions. The reason for this was only recently discovered. The increase in sebum production is beneficial for the virulent phylotypes of C. acnes as these have higher triglyceride lipase activity and can digest sebum much more effectively than the neutral phylotypes of C. acnes. In that sense, the virulent phylotypes have a genetic advantage which allows them to grow and start dominating the hair follicle when sebum production is elevated (Fig 1). The virulent C. acnes phylotypes are more


active in producing mediators which induce inflammation. This is an important feature in the formation of acne lesions. Another important feature is the fact that the virulent phylotypes are very active in producing biofilm. A biofilm is an organized conglomerate of bacterial cells attached to a surface and embedded into a self-produced matrix composed of polysaccharides. This protective shell forms a barrier allowing virulent C. acnes to survive in harsh environments and multiply. An important new finding is that the biofilm acts as a ‘glue’ which, together with dead skin cells, clogs the pores. This is important, as this will make the environment in the hair follicles even more favorable for virulent, and anaerobic, C. acnes (Fig 2). Their high triglyceride lipase activity


allows virulent C. acnes phylotypes to not just grow but also produce large amounts of free fatty acids, many of which have an important negative impact on the surrounding hair


100 90 80 70 60 50 40 30 20 10 0


Figure 5: Reduction of gene expression of different types of 5-reductase by LPM Complex. Control


Type 1 Type 2 Type 3


follicle. Oleic acid is an example of such a molecule. Essentially the triglycerides from sebum are digested by lipase. The glycerin is used by C. acnes and many of the remaining free fatty acids are excreted. Oleic acid plays multiple negative roles that are crucial in the formation of papules and pustules. It has a negative impact on the keratinocytes surrounding the hair follicle, for instance. Their barrier function is strongly reduced and the accompanying stress leads to the instigation of inflammation in these cells. Oleic acid allows virulent C. acnes to further adhere to the hair follicle and produce more biofilm (Fig 3). The above-described processes are


essential at the start of a vicious circle, where virulent C. acnes grows and forms biofilm while, directly and indirectly, inducing inflammation and eventually leading to the


formation of acne lesions. In order to reduce the likelihood of the formation of acne lesions addressing sebum production, growth of virulent phylotypes of C. acnes and biofilm formation by these phylotypes are essential. Acne is, in essence, an inflammatory


problem. Papules are small red, tender bumps, and pustules are papules filled with pus. Both are inflammatory lesions, and in order to actively fight acne, the inflammatory processes in these lesions need to be reduced. The inflammatory processes induced by


virulent C. acnes start locally, but are quickly amplified, with keratinocytes and fibroblasts in the surrounding dermis playing an important role. The formation of papules and pustules, however, is a consequence of the invasion of immune cells, which is a


October 2020


PERSONAL CARE NORTH AMERICA


Gene expression (%)


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