Propionibacterium is a gram-positive, anaerobic, rod-shaped genus of bacteria named for their unique metabolism: They are able to synthesize propionic acid by using unusual transcarboxylase enzymes.
|Cutibacterium (formerly Propionibacterium) acnes|
Its members are primarily facultative parasites and commensals of humans and other animals, living in and around the sweat glands, sebaceous glands, and other areas of the skin. They are virtually ubiquitous and do not cause problems for most people, but propionibacteria have been implicated in acne and other skin conditions. One study found the Propionibacterium was the most prevalent human skin-associated genus of microorganisms.
Propionibacterium spp. are commensal bacteria that can occasionally cause infectious diseases. The most studied of these infections is acne vulgaris, caused by Cutibacterium acnes (formerly Propionibacterium acnes). It is a chronic inflammatory disease caused by the blockage of pilosebaceous units causing inflammatory lesions, non-inflammatory lesions or a mixture of both on the face, neck and/or chest. Acne vulgaris cannot be defined as an infectious disease since the bacteria is found on a vast majority of individuals without causing lesions. C. acnes colonize the skin only under certain favorable conditions. In most cases, C. acnes get trapped under the comedones where they proliferate to form micro-comedones, not visible to the naked eye, which can later form structures such as closed comedones (white heads) and open comedones. These comedones can rupture, releasing the follicular material inside the dermis. The cause of this rupture was thought to be the indirect effect of fat metabolism by the bacteria, however it was later found that bacteria are directly involved in comedome rupturing by producing factors such as proteases, hyaluronidases and neuraminidases which might be involved in thinning of the epithelium. C. acnes can also produce immune factors such as proinflammatory cytokine inducing-factors and chemotactic factors, and can induce host complement pathways.
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