&lt;b&gt;&lt;i&gt;Staphylococcus epidermidis&lt;/i&gt;&lt;/b&gt;: A Potential New Player in the Physiopathology of Acne?

Claudel, Jean‐Paul; Auffret, N.; Leccia, Marie‐Thérèse; Poli, F.; Corvec, Stéphane; Dréno, Brigitte

doi:10.1159/000499858

Cited by 121 publications

(95 citation statements)

References 77 publications

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“…epidermidis was the second most prevalent microbiota (19%) before treatment and became the most prevalent bacteria (28%) after treatment. S. epidermidis and C. acnes use glycerol as a shared carbon source to generate different short-chain fatty acids used as antimicrobial agents to compete against each other [26]. Different in vivo antagonism investigations demonstrated that S. epidermidis controls the proliferation of C. acnes via the release of succinic acid, a fatty acid fermentation product, which blocks surface toll-like receptors (TLRs) of keratinocytes and tumor necrosis factor and suppresses C. acnes-induced IL-6 [27][28][29].…”

Section: Discussionmentioning

confidence: 99%

Characterization and Analysis of the Skin Microbiota in Acne: Impact of Systemic Antibiotics

Park

Kim

Lee

et al. 2020

JCM

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Systemic antibiotics are extensively used to control moderate to severe acne. Hence, it is crucial to understand their impact on the skin microbiota, which is supposedly perturbed. The purpose of this study was to compare the makeup and diversity of the skin microbiota in acne patients before and after taking oral antibiotics. A longitudinal cohort study was performed on 20 participants with moderate to severe facial acne with no recent use of oral and topical antibiotics/retinoids. Patients were prescribed oral doxycycline, 100 mg, twice daily for six weeks. Skin areas on the cheek were sampled for 16S ribosomal RNA gene sequencing at baseline, and after six weeks of doxycycline treatment. Ten males and 10 females aged 11 to 44 years with a median Investigator’s Global Assessment score of 3 (moderate) were enrolled. At baseline, Cutibacterium acnes (formerly Propionibacterium acnes) was the most dominant species followed by Staphylococcus epidermidis. Acne severity showed a positive correlation with the abundance of Cutibacterium acnes. Across all subjects, antibiotic treatment reduced clinical acne grades and was associated with a 1.96-fold reduction in the relative abundance of Cutibacterium acnes (p = 0.01, 95% CI −22% to −3%). Marked changes were also identified in other bacterial species, such as Cutibacterium granulosum (formerly Propionibacterium granulosum), which increased by 4.46-fold (p = 0.02, 95% CI 0.004% to 0.9%) in the treated samples. In general, antibiotics administration was associated with an increase in bacterial diversity (alpha diversity). Principal coordinates analysis showed mild clustering of samples by patient (analysis of similarity, R = 0.135, p = 0.04) whereas there was scant clustering with treatment (ANOSIM, R = 0.005; p = 0.29). In conclusion, we found individuals with acne to have a unique microbial signature. Acne treatment with systemic antibiotics was associated with changes in the composition and diversity of skin microbiota, especially Cutibacterium acnes, which correlates with acne severity. Our study provides insight into the skin microbiota in acne and how it is modulated by systemic antibiotics.

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Section: Discussionmentioning

confidence: 99%

Characterization and Analysis of the Skin Microbiota in Acne: Impact of Systemic Antibiotics

Park

Kim

Lee

et al. 2020

JCM

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“…For example, some C. acnes phylogroups encode biosynthesis genes for a thiopeptide with possible antimicrobial activity against S. epidermidis, which conversely secretes bacteriocins such as epidermin that kills C. acnes 32 . The antagonism between S. epidermidis and C. acnes is also noted in acne vulgaris, in which not only SCFAs but many factors like antimicrobial peptides secreted from keratinocytes have an impact 33 . Considering that S. epidermidis also produces SCFAs, further study of additional, unidentified factors other than SCFAs should be addressed in the future.…”

Section: Control Scfasmentioning

confidence: 99%

Short chain fatty acids produced by Cutibacterium acnes inhibit biofilm formation by Staphylococcus epidermidis

Nakamura

O’Neill

Williams

et al. 2020

Sci Rep

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Biofilm formation by bacterial pathogens is associated with numerous human diseases and can confer resistance to both antibiotics and host defenses. Many strains of Staphylococcus epidermidis are capable of forming biofilms and are important human pathogens. Since S. epidermidis coexists with abundant Cutibacteria acnes on healthy human skin and does not typically form a biofilm in this environment, we hypothesized that C. acnes may influence biofilm formation of S. epidermidis. Culture supernatants from C. acnes and other species of Cutibacteria inhibited S. epidermidis but did not inhibit biofilms by Pseudomonas aeruginosa or Bacillus subtilis, and inhibited biofilms by S. aureus to a lesser extent. Biofilm inhibitory activity exhibited chemical properties of short chain fatty acids known to be produced from C. acnes. The addition of the pure short chain fatty acids propionic, isobutyric or isovaleric acid to S. epidermidis inhibited biofilm formation and, similarly to C. acnes supernatant, reduced polysaccharide synthesis by S. epidermidis. Both short chain fatty acids and C. acnes culture supernatant also increased sensitivity of S. epidermidis to antibiotic killing under biofilm-forming conditions. These observations suggest the presence of C. acnes in a diverse microbial community with S. epidermidis can be beneficial to the host and demonstrates that short chain fatty acids may be useful to limit formation of a biofilm by S. epidermidis.

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“…n -Butyric acid ( 47 ) is a short-chain fatty acid reported as metabolite of Staphylococcus epidermidis , a skin probiotic bacterium ( Claudel et al, 2019 ; Traisaeng et al, 2019 ). n -butyric acid has been reported to inhibit HDAC, DNA synthesis, and cell growth in colon tumor cell lines ( Andriamihaja et al, 2009 ; Zhang et al, 2010 ; Traisaeng et al, 2019 ).…”

Section: Hdac Inhibitorsmentioning

confidence: 99%

Natural Products Impacting DNA Methyltransferases and Histone Deacetylases

et al. 2020

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Epigenetics refers to heritable changes in gene expression and chromatin structure without change in a DNA sequence. Several epigenetic modifications and respective regulators have been reported. These include DNA methylation, chromatin remodeling, histone post-translational modifications, and non-coding RNAs. Emerging evidence has revealed that epigenetic dysregulations are involved in a wide range of diseases including cancers. Therefore, the reversible nature of epigenetic modifications concerning activation or inhibition of enzymes involved could be promising targets and useful tools for the elucidation of cellular and biological phenomena. In this review, emphasis is laid on natural products that inhibit DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) making them promising candidates for the development of lead structures for anticancer-drugs targeting epigenetic modifications. However, most of the natural products targeting HDAC and/or DNMT lack isoform selectivity, which is important for determining their potential use as therapeutic agents. Nevertheless, the structures presented in this review offer the well-founded basis that screening and chemical modifications of natural products will in future provide not only leads to the identification of more specific inhibitors with fewer side effects, but also important features for the elucidation of HDAC and DNMT function with respect to cancer treatment.

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<b><i>Staphylococcus epidermidis</i></b>: A Potential New Player in the Physiopathology of Acne?

Cited by 121 publications

References 77 publications

Characterization and Analysis of the Skin Microbiota in Acne: Impact of Systemic Antibiotics

Characterization and Analysis of the Skin Microbiota in Acne: Impact of Systemic Antibiotics

Short chain fatty acids produced by Cutibacterium acnes inhibit biofilm formation by Staphylococcus epidermidis

Natural Products Impacting DNA Methyltransferases and Histone Deacetylases

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