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The proteins and lipids produced by Cutibacterium acnes comprise a diverse group of molecules central to the bacterium’s adaptation to human skin and its role in health and disease. Key proteins include multiple lipases, such as triacylglycerol lipase GehA and GehB, which degrade sebum triglycerides into free fatty acids, modulating skin pH and inflammation and contributing to acne pathogenesis[9]. The lipid profile includes triglycerides, ceramides, phosphatidylcholine, sphingomyelins, cardiolipins, and fatty acid amides, with unique lipids serving as potential strain markers for diagnostics and epidemiology[4][2][5]. Bacterial metabolites such as propionic acid shape both the microbiome and epidermal lipid synthesis, enhancing barrier function but also promoting colonization and sometimes inflammation[1][3][7]. Both proteins and lipids can serve as antigens, modulate host immunity, and have therapeutic and diagnostic significance in skin diseases and infections. If a more specific molecular target is required, “Cutibacterium acnes triacylglycerol lipase (GehA)” or “Cutibacterium acnes ceramide” would be preferred canonical entries[9][2][5].
Enzyme inhibition (inhibition of lipase activity to prevent lipid degradation and FFA-driven inflammation) Bactericidal action (antibiotics disrupt bacterial cell wall or protein synthesis) Modulation of lipid metabolism (drugs that alter keratinocyte lipid synthesis, affecting colonization and barrier function)
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