Ontology highlight
ABSTRACT:
PROVIDER: PRJNA714802 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cutibacterium avidum isolated from prosthetic hip joint infections
| PRJNA1045027 | ENA
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.
2022-05-20 | PXD025460 | Pride
Project description:In the present study, we investigated the effect of Cutibacterium acnes on lifespan and susceptibility to infection with Staphylococcus aureus using Caenorhabditis elegans as a model animal. When adult C. elegans were fed C. acnes strains, the lifespan of the animals fed pathogenic C. acnes strain (HM-122) was significantly shorter than that of animals fed OP50 (control). In contrast, the lifespan of the animals fed commensal C. acnes strain (HM-555) was not significantly different from that of animals in the control group. Moreover, the worms fed the commensal C. acnes strain were more resistant to infection with S. aureus. Transcriptional profiling comparing HM-122-, HM-555- and control-fed animals suggested that genes related to “cuticle development involved in collagen and cuticulin-based cuticle molting cycle” were regulated by HM-122, and genes related to “defense response to gram-positive bacterium” were regulated by HM-555.
2021-10-07 | GSE176406 | GEO
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:Proprionibacterium acnes is a Gram positive bacterium found ubiquitously on human skin, where it is typically considered to assume a commensal relationship with its host. However, it is also closely associated with the skin condition acne vulgaris. More controversially, it has a postulated involvement in infections of implanted prosthetic devices and has been isolated from malignant prostate tissues. The role of P. acnes in these pathologies remains undetermined, although both bacterial and host factors are implicated. By microarray analysis, we have identified fundamental differences in the global transcriptional profiles of keratinocyte and prostate cells to P. acnes infection. Notably, P. acnes infection of the keratinocyte cell line, HaCaT, elicited a robust, but acute inflammatory response. By contrast, the inflammatory response of the prostate cell line, RWPE1, was delayed and persisted for longer times. Immunofluorescence and electron microscopy revealed higher numbers of internalized P. acnes bacteria in RWPE1 cells, which could still be detected intracellularly three weeks post infection. This contrasted with HaCaT cells, which P. acnes largely failed to invade. Moreover, P. acnes induced a delayed, sustained activation of NFM-NM-:B in RWPE1 cells, which was absent in HaCaT cells. Further characterization of the host-cell response to infection revealed that the intermediate filament protein, vimentin, was a key determinant of P. acnes invasion, persistence and inflammatory profile in RWPE1 cells. siRNA mediated knock down of vimentin in RWPE1 cells attenuated bacterial invasion and the inflammatory response to infection; similarly, overexpression of vimentin in HaCaT cells increased bacterial invasion. We conclude that vimentin-dependent host-tissue tropism, in part, determines P. acnes invasion and inflammatory capacity. This could contribute to P. acnes pathology at non-skin infection sites. Microarray experiments were performed as dual-color hybridizations. In order to compensate specific effects of the dyes and to ensure statistically relevant data analysis, a color-swap dye-reversal was performed.
2012-11-21 | E-GEOD-33731 | biostudies-arrayexpress
Project description:Cutibacterium acnes is a predominant member of the human skin microbiome that plays a pivotal role in maintaining homeostasis and protecting the host against pathogen colonization. Staphylococcus lugdunensis, while also a resident of the skin microbiota, is an opportunistic pathogen capable of causing severe infections, associated with its ability to form biofilms. Building on our previous observation that C. acnes secretes molecules capable of inhibiting S. lugdunensis biofilm formation without inhibiting planktonic growth, we investigated the underlying molecular mechanisms of this phenomenon. Here, we demonstrate that cell-free supernatants from various C. acnes strains exhibit dose-dependent antibiofilm activity targeting the initial stages of S. lugdunensis biofilm development. Additionally, extracellular molecules from C. acnes cultures significantly reduced the ability of S. lugdunensis to adhere to and invade human epithelial cells (A549) and to adhere to keratinocytes (HaCaT). Transcriptomic analysis revealed that C. acnes-derived molecules significantly repressed the expression of genes involved in purine biosynthesis in S. lugdunensis, while inducing the expression of the negative regulators of autolysis, lrgA and lrgB. Functional assays confirmed that C. acnes-derived molecules inhibit autolysis and extracellular DNA (eDNA) release by S. lugdunensis. Crucially, the addition of exogenous guanine suppressed the effect of C. acnes molecules on both biofilm formation and lrgA gene expression. Collectively, our data indicate that C. acnes molecules inhibit S. lugdunensis biofilm formation by depleting the intracellular guanine pool, which leads to repression of autolysis, thereby reducing the release of eDNA essential for biofilm structural integrity. These findings underscore the potential of exploiting interspecies microbiome interactions to better understand their role in pathogen exclusion.
2026-04-30 | GSE327969 | GEO
Project description:Cutibacterium acnes isolates from severe infections
| PRJEB52145 | ENA