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Engineering selectivity of Cutibacterium acnes phages by epigenetic imprinting

ABSTRACT: Engineering selectivity of Cutibacterium acnes phages by epigenetic imprinting

PROVIDER: PRJEB42527 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR10787787_1.fastq.gz	Fastqsanger.gz
	ERR10787787_2.fastq.gz	Fastqsanger.gz
	ERR10787788_1.fastq.gz	Fastqsanger.gz
	ERR10787788_2.fastq.gz	Fastqsanger.gz

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Engineering selectivity of Cutibacterium acnes phages by epigenetic imprinting.

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Project description:Recently the membrane vesicles (MVs) production has been observed in Gram-positive bacterium, Cutibacterium acnes (C. acnes). In order to explore the mechanism of antibiotic resistance and the virulent components within the C. acnes-derived MVs, we isolated MVs from the clinical C. acnes, which were sensitive or resistant to antibiotics erythromycin and clindamycin. With the LC-MS/MS method, we detected several lipases, virulent factors and cell division protein differentially expressed between the sensitive and the resistant C. acnes-derived MVs.

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Molecular typing and functional profiling of acne-derived Cutibacterium acnes isolates reveal determinants of skin inflammation

Project description:Cutibacterium acnes (C. acnes) is a ubiquitous skin commensal bacterium that is generally well tolerated by the immune system. Different strain-types of C. acnes have been reported to be enriched on patients with acne. To understand if these strain-types contribute to skin inflammation, we generated a library of over 200 C. acnes isolates from skin swabs of healthy and acne subjects and assessed their strain-level identity and inflammatory potential. Phylotype II K-type strains were more frequent on healthy and acne non-lesional skin compared to lesional. Phylotype IA-1 C-type strains were dominant on acne lesional skin but absent from healthy. Measurement of host cytokine responses from C. acnes supernatant revealed neither strain-type nor skin-type association predicted inflammatory potential. However, differential proinflammatory responses were induced from identical strain-types, but these differences were not attributable to protease, short chain fatty acid or porphyrin production. Instead, whole genome sequencing revealed the presence of a linear plasmid in high inflammatory strain-types. Intradermal injection of C. acnes in mouse skin revealed a plasmid-associated inflammatory response in dermal fibroblasts, revealed by single-cell RNA sequencing. We conclude that C. acnes strain-type is not sufficient to predict inflammation but other virulence factors including a plasmid may contribute to disease.

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