Abstract
Cutibacterium acnes is a member of the skin microbiota found predominantly in regions rich in sebaceous glands. It is involved in maintaining healthy skin and has long been considered a commensal bacterium. Its involvement in various infections has led to its emergence as an opportunist pathogen. Interactions between C. acnes and the human host, including the human skin microbiota, promote the selection of C. acnes strains capable of producing several virulence factors that increase inflammatory capability. This pathogenic property may be related to many infectious mechanisms, such as an ability to form biofilms and the expression of putative virulence factors capable of triggering host immune responses or enabling C. acnes to adapt to its environment. During the past decade, many studies have identified and characterized several putative virulence factors potentially involved in the pathogenicity of this bacterium. These virulence factors are involved in bacterial attachment to target cells, polysaccharide-based biofilm synthesis, molecular structures mediating inflammation, and the enzymatic degradation of host tissues. C. acnes, like other skin-associated bacteria, can colonize various ecological niches other than skin. It produces several proteins or glycoproteins that could be considered to be active virulence factors, enabling the bacterium to adapt to the lipophilic environment of the pilosebaceous unit of the skin, but also to the various organs it colonizes. In this review, we summarize current knowledge concerning characterized C. acnes virulence factors and their possible implication in the pathogenicity of C. acnes.
Highlights
Cutibacterium acnes is a member of the skin microbiota found predominantly in regions rich in sebaceous glands
Genus Cutibacterium belongs to a branch of Actinobacter and can be split into two groups, one containing the so-called “classic or dairy” species, bringing together saprophytic species isolated from non-human-pathogenic dairy products, and the other containing commensal “skin” species, most found on the surface of human skin
Antibiotics were found to be effective against inflammatory acne, but the selection pressure exerted by antibiotic treatment for this condition has led to the induction of antibiotic resistance in up to 40% of C. acnes strains, increasing the likelihood of treatment failure [11]
Summary
Lipase are the enzymes responsible for metabolizing sebum and releasing free fatty acids (FFAs) in the PSU, in addition to several different triglycerides [119,120]. A triacylglycerol lipase (glycerol-ester hydrolase A: GehA) secreted by C. acnes has been identified, together with GehB, which appears to be present in large amounts in human sebaceous follicles [116,122,123]. The genome of C. acnes encodes at least 12 putative lipases, including GehA and GehB, both of which carry a signal peptide, consistent with their secretion. Lipases, including GehA in particular, were the first molecules identified as putative C. acnes virulence factors, because they can generate FFAs through the degradation of sebum lipids, thereby promoting inflammation. Lipases appear to play a determinant role in the growth of C. acnes in lipophilic environments. Their conformational structure may depend of the lipid level inside the PSU and could influence the pathogenicity of the strain
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