Cutibacterium acnes KPA171202
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ABSTRACT:
PROVIDER: PRJNA12460 | ENA |
REPOSITORIES: ENA
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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.
2023-08-18 | GSE211279 | GEO
Project description:Cutibacterium acnes (C. acnes) is a common skin commensal associated with acne pathogenesis. Here, we investigated the capacity of acne-associated (CA) and healthy skin-associated (CH) C. acnes strains to induce extracellular trap (ET) formation in human neutrophils (NETs) and Th17 cells (TETs) and performed proteomic analyses to define their molecular signatures. NETs displayed a conserved protein profile regardless of the C. acnes strain, whereas TETs exhibited strain-specific proteomic profiles. CA-induced TETs were enriched in inflammatory and extracellular matrix remodeling proteins, while CH-induced TETs showed upregulation of nuclear, mitochondrial, and antimicrobial proteins, including granulysin, granzyme B, and cathepsin C. These findings underscore strain- and cell type-specific regulation of ET formation and suggest that CH-induced TETs may contribute to skin immune homeostasis, whereas CA-induced TETs may promote inflammatory and tissue remodeling responses in acne. Our study reveals a potential mechanism by which skin microbiota differentially modulates Th17 effector programs, ultimately influencing downstream immune activity and skin health.
2026-02-09 | MSV000100784 | MassIVE
Project description:Acne vulgaris is a chronic inflammatory dermatosis where conventional therapies of-ten face limitations in efficacy and safety, necessitating the development of microbi-ome-targeted interventions. This study investigated the immunomodulatory potential of microbiome-derived tryptophan metabolites as a novel therapeutic strategy for Cutibacterium acnes-induced inflammation, focusing on the aryl hydrocarbon receptor (AHR) pathway. We evaluated indole-3-lactic acid (ILA), indole-3-acrylic acid (IAA), and indole-3-propionic acid (IPA) in comparison to tapinarof, utilizing C. ac-nes-stimulated human epidermal keratinocytes and a C. acnes-induced acne mouse model. In vitro, ILA and IPA significantly suppressed C. acnes-driven inflammatory mediators, including TNF-α, IL-1β, and COX2, whereas IAA demonstrated limited ef-ficacy. In vivo, ILA treatment exhibited superior therapeutic activity, markedly reduc-ing inflammatory cell infiltration, epidermal hyperplasia, and IL-1β expression. Tran-scriptomic analysis confirmed that ILA attenuates inflammatory signaling (e.g., IL-17 and TNF pathways) while upregulating AHR-responsive genes such as CYP1A1 and CYP1B1. Collectively, these findings establish ILA as a potent postbiotic that mitigates cutaneous inflammation through selective activation of the AHR. Future studies should prioritize the clinical translation of ILA-based topical fomulations, with rigorous evaluation of their efficacy and safety in well-designed human trials, to support their development as a non-antibiotic therapeutic alternative for acne management.
2026-01-05 | GSE315350 | GEO
Project description:The pathogenesis of acne vulgaris is multifactorial and is influenced by the presence of Cutibacterium acnes. This study investigated how different strains of C. acnes, associated with either healthy skin (CH) or acne-prone skin (CA), selectively modulate the function of three dendritic cell (DC) subtypes: Langerhans cell-derived (LCDC), monocyte-derived (moDCs), and myeloid (mDCs). Our findings revealed that all DC subtypes secreted varying levels of TGF-β, IL-1β, IL-6, IL-12p70, and IL-23 in response to C. acnes stimulation. Notably, moDCs exhibited the highest cytokine secretion in response to CA-ribotypes, indicating their potent immune responsiveness. Conversely, LCDCs were the least responsive, regardless of the ribotypes. Principal component (PCA) and gene ontology (GO) analysis of bulk RNA sequencing data of DCs exposed to C. acnes identified extensive transcriptional changes, particularly in immune response pathways. moDCs showed the most pronounced transcriptional changes, aligning with their high cytokine secretion levels. Additionally, we identified specific genes upregulated by CA-ribotypes, with notable differences among the DC types, highlighting the unique contributions of each DC subtype to the skin's immune defense mechanisms against C. acnes. Overall, our study underscores the complexity of DC responses in the skin's immune environment and provides valuable insights into their roles in acne.
2025-02-01 | GSE255918 | GEO
Project description:TRPV3 is highly expressed in human skin and is involved in the development of inflammatory dermatoses. However, it remains unclear whether TRPV3 influences inflammation in human sebaceous glands and its role in the pathogenesis of acne. Here, we showed that TRPV3 expression was increased in the sebaceous glands of facial acne lesions and acne-like mice. TRPV3 increased the secretion of pro-inflammatory cytokines and chemokines in human SZ95 sebocytes, as well as the chemotaxis of neutrophils, which were the major immune cells found in acne lesions. We demonstrated that P.acnes promoted TRPV3 expression through regulating lipid profile especially upregulated arachidonic acid levels in human sebocytes. TRPV3 further upregulated TLR2 expression by promoting transcriptional factor p-FOSL1 expression and its binding to the TLR2 promoter, leading to downstream NF-κB signaling activation. Importantly, either genetic silencing or pharmacological inhibition of TRPV3 alleviated acne-like inflammation in mice, showing reduced acne-characteristic cytokines and chemokines production and neutrophil infiltration by inhibiting the TLR2-NF-κB axis. Thus, our study revealed the critical role of TRPV3 in sebocytes inflammation, which was involved in the development of acne, indicating that TRPV3 is a potential therapeutic target for acne and other disorders of the pilosebaceous unit.
2023-10-13 | GSE245001 | GEO
Project description:Comparative analysis of Cutibacterium acnes extracellular vesicles proteomics from atopic dermatitis and acne vulgaris.
2023-06-03 | PXD042715 |
Project description: Not available
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