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willow569

p. acnes may be involved in microcomedone development

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Interesting article that indicates p. acnes is involved in both the inflammation of acne lesions and also in microcomedone development. I’m attaching the full article – it’s a bit technical, but it’s still worth a read through. There is some interesting discussion about how this is a local stress response in the skin, similar to the hormonal stress responses seen systemically throughout the body. It would explain a lot of things – like the link between stress and acne, and the reason that BPO is effective for preventing noninflamed acne. It also talks about the role of zinc for reducing inflammation.

http://www.ncbi.nlm.nih.gov/pmc/articles/P...98/?tool=pubmed

Dermatoendocrinol. 2009 Mar;1(2):96-9.

Cutaneous induction of corticotropin releasing hormone by Propionibacterium acnes extracts.

Isard O, Knol AC, Castex-Rizzi N, Khammari A, Charveron M, Dréno B.

The skin commensal bacillus Propionibacterium acnes is known to play a major role in the development of acne vulgaris and it is established that this bacteria is involved both in the induction and maintenance of the inflammatory phase of acne. The corticotropin releasing hormone (CRH), a neuropeptide originally isolated from the hypothalamus, is also produced by the skin. CRH has been reported to play a role in the inflammation, the production of sebum and finally the differentiation of keratinocytes. At the therapeutic level, zinc is known to act specifically on inflammatory lesions with still partially known mechanisms and thus could play an important role in the development of inflammatory acne lesions. Our objective was to study the modulation of CRH expression by keratinocytes induced by P. acnes extracts. CRH expression was examined using immunohistochemistry technique on deep-frozen sections of normal human skin explants incubated with two different extracts of P. acnes and with or without zinc salts. We observed that the membrane fraction (FM) of P. acnes increased the CRH expression in the epidermis. This result indicates that P. acnes, by stimulating the production of CRH, can both modulate the differentiation of keratinocytes and increase the local inflammation, arguing that this bacterium plays a role not only in the development of inflammatory acne lesions but also in the formation of the microcomedo in the early stages of acne. In this study, we demonstrate for the first time that P. acnes acts as a strong local stressor at the origin of CRH overexpression by keratinocytes, in the epidermis. Thus, as CRH modifies the differentiation of keratinocytes, we confirm that this bacterium has a spectrum of action, not limited to inflammation but also in the early stages of the formation of acne lesions.29 This confirms the fundamental role played by this bacterium which can be detected as a local stressor by the skin and could potentially lead to the development of acne lesions.

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Interesting. That's why for many people with even non-inflammatory acne, BP seems to be more effective than SA, since SA doesn't kill P acnes.

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Interesting. That's why for many people with even non-inflammatory acne, BP seems to be more effective than SA, since SA doesn't kill P acnes.

Yeah - most people (and many doctors) underestimate the ability of BPO to treat noninflammatory forms of acne. So, based on the theory presented in this article, BPO may help prevent the formation of the microcomedone, the start of the majority of acne lesions.

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