Propionibacterium acnes – disease causing agent or common contaminant? Detection in diverse patient samples by next generation sequencing
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ABSTRACT:
PROVIDER: PRJEB12636 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1248510.fastq.gz | Fastqsanger.gz | |||
| ERR1248520.fastq.gz | Fastqsanger.gz | |||
| ERR1248530.fastq.gz | Fastqsanger.gz | |||
| ERR1248540.fastq.gz | Fastqsanger.gz | |||
| ERR1248550.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Propionibacterium acnesis the most abundant bacterium on human skin, particularly in sebaceous areas.P. acnesis suggested to be an opportunistic pathogen involved in the development of diverse medical conditions but is also a proven contaminant of human clinical samples and surgical wounds. Its significance as a pathogen is consequently a matter of debate. In the present study, we investigated the presence ofP. acnesDNA in 250 next-generation sequencing data sets generated from 180 samples of 20 different sample types, mostly of cancerous origin. The samples were subjected to either microbial enrichment, involving nuclease treatment to reduce the amount of host nucleic acids, or shotgun sequencing. We detected high proportions ofP. acnesDNA in enriched samples, particularly skin tissue-derived and other tissue samples, with the levels being higher in enriched samples than in shotgun-sequenced samples.P. acnesreads were detected in most samples analyzed, though the proportions in most shotgun-sequenced samples were low. Our results show thatP. acnescan be detected in practically all sample types when molecular methods, such as next-generation sequencing, are employed. The possibility of contamination from the patient or other sources, including laboratory reagents or environment, should therefore always be considered carefully whenP. acnesis detected in clinical samples. We advocate that detection ofP. acnesalways be accompanied by experiments validating the association between this bacterium and any clinical condition.
| S-EPMC4809928 | biostudies-literature
Project description:Prostate cancer is the second leading cause of male cancer deaths in the United States and Europe. Current evidence implicates an inflammatory mechanism as a cause of prostate carcinogenesis. Here we show that the bacterium Propionibacterium acnes (P. acnes) is prevalent in prostate glandular tissues: 70% of benign hyperplasia and 81% of cancer tissue samples tested positive for the bacterium. Live P. acnes bacteria were isolated from cancerous prostates and co-cultured with epithelial prostate cells to confirm they were cell invasive. Transcriptome and ELISA studies revealed that P. acnes induced a strong inflammatory response in prostate cells, resulting in the secretion of cytokines and chemokines such as interleukin (IL)-6 and IL-8. In addition, P. acnes triggered the COX prostaglandin and the plasminogen-matrix metalloproteinase (MMP) pathways. Strikingly, long-term exposure of non-tumorigenic prostate cells to P. acnes resulted in loss of E-cadherin, altered betacatenin levels and localization, increased cellular migration, and conferred anchorage- independent growth. Our work adds to the growing body of work highlighting the presence of viruses and bacteria in cancerous prostate tissues and strongly suggests that P. acnes infection could lead to malignant transformation of prostate cells.
2010-12-22 | GSE18109 | GEO
Project description:Prostate cancer is the second leading cause of male cancer deaths in the United States and Europe. Current evidence implicates an inflammatory mechanism as a cause of prostate carcinogenesis. Here we show that the bacterium Propionibacterium acnes (P. acnes) is prevalent in prostate glandular tissues: 70% of benign hyperplasia and 81% of cancer tissue samples tested positive for the bacterium. Live P. acnes bacteria were isolated from cancerous prostates and co-cultured with epithelial prostate cells to confirm they were cell invasive. Transcriptome and ELISA studies revealed that P. acnes induced a strong inflammatory response in prostate cells, resulting in the secretion of cytokines and chemokines such as interleukin (IL)-6 and IL-8. In addition, P. acnes triggered the COX prostaglandin and the plasminogen-matrix metalloproteinase (MMP) pathways. Strikingly, long-term exposure of non-tumorigenic prostate cells to P. acnes resulted in loss of E-cadherin, altered betacatenin levels and localization, increased cellular migration, and conferred anchorage- independent growth. Our work adds to the growing body of work highlighting the presence of viruses and bacteria in cancerous prostate tissues and strongly suggests that P. acnes infection could lead to malignant transformation of prostate cells. Microarray experiments were performed as dual-color hybridizations. To compensate for dye-specific effects, a dye-reversal color-swap was applied. Ratio profiles comprising color-swap hybridizations were combined in an error-weighted fashion to create ratio experiments. A 1.5–fold change expression cut-off for ratio experiments was applied together with anti-correlation of color-swap ratio profiles rendering the microarray analysis highly significant (P-value > 0.01), robust and reproducible.
2010-12-22 | E-GEOD-18109 | biostudies-arrayexpress
Project description:The anaerobic Gram-positive bacterium Propionibacterium acnes is a human skin commensal, but is occasionally associated with inflammatory diseases. Recent work has indicated that evolutionary distinct lineages of P. acnes play etiologic roles in disease while others are associated with health. To shed light on the molecular basis for differential strain properties, we carried out genomic and transcriptomic analysis of distinct P. acnes strains. We sequenced the genome of the P. acnes strain 266, a type I-1a sequence type (ST) 18 strain. Comparative genome analysis of strain 266 and four other P. acnes strains revealed that overall genome plasticity is relatively low; however, a number of island-like genomic regions, encoding a variety of putative virulence-associated and fitness traits, differ between phylotypes. Comparative transcriptome analysis revealed that 225 genes of strain KPA171202 (type I-2, ST34) were differentially transcribed in strain 266 during exponential growth. 47% of these genes belong to the strain-specific gene content of strain KPA171202, indicating that strain-specific functions are utilized. Next, we studied differential expression during exponential and stationary growth phases. Genes encoding components of the energy-conserving respiratory chain as well as secreted and virulence-associated factors were transcribed during the exponential phase, while the stationary growth phase was characterized by up-regulation of genes involved in the stress response and amino acid metabolism. Taken together, our data highlight the genomic basis for strain diversity and identify, for the first time, the transcribed part of the genome, underling the important role active growth plays in the inflammatory activity of P. acnes. We argue that the disease-causing potential of different P. acnes strains is not only determined by variable genome content but also, and to a greater degree, by variable transcriptomes.
2011-07-01 | GSE26738 | GEO
Project description:The anaerobic Gram-positive bacterium Propionibacterium acnes is a human skin commensal, but is occasionally associated with inflammatory diseases. Recent work has indicated that evolutionary distinct lineages of P. acnes play etiologic roles in disease while others are associated with health. To shed light on the molecular basis for differential strain properties, we carried out genomic and transcriptomic analysis of distinct P. acnes strains. We sequenced the genome of the P. acnes strain 266, a type I-1a sequence type (ST) 18 strain. Comparative genome analysis of strain 266 and four other P. acnes strains revealed that overall genome plasticity is relatively low; however, a number of island-like genomic regions, encoding a variety of putative virulence-associated and fitness traits, differ between phylotypes. Comparative transcriptome analysis revealed that 225 genes of strain KPA171202 (type I-2, ST34) were differentially transcribed in strain 266 during exponential growth. 47% of these genes belong to the strain-specific gene content of strain KPA171202, indicating that strain-specific functions are utilized. Next, we studied differential expression during exponential and stationary growth phases. Genes encoding components of the energy-conserving respiratory chain as well as secreted and virulence-associated factors were transcribed during the exponential phase, while the stationary growth phase was characterized by up-regulation of genes involved in the stress response and amino acid metabolism. Taken together, our data highlight the genomic basis for strain diversity and identify, for the first time, the transcribed part of the genome, underling the important role active growth plays in the inflammatory activity of P. acnes. We argue that the disease-causing potential of different P. acnes strains is not only determined by variable genome content but also, and to a greater degree, by variable transcriptomes. 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. Two different labeling methods were applied. RNA labeling was performed with the two color Quick Amp Labeling Kit (Agilent Technologies) using FullSpectrum MultiStart Primer for T7 IVT RNA Amplification (BioCat GmbH, Heidelberg, Germany) as random T7 labeling. Alternatively, the total RNA samples were amplified with the TransPlex Whole Transcriptome Amplification Kit (Sigma-Aldrich, Munich, Germany) and labeled with BioPrime Plus Array CGH Indirect Genomic Labeling System (Invitrogen, Karlsruhe, Germany) as WTA BioPrime indirect. Both methods were compared and combined for final data analysis.
2011-07-01 | E-GEOD-26738 | biostudies-arrayexpress
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 NFκB 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.
2012-11-21 | GSE33731 | 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:Individual acne comedones can undergo spontaneous remission in association with shrunken sebaceous glands (SGs) containing undifferentiated cells under unknown mechanisms. It is also still controversial whether sebum-induced follicular Propionibacterium acnes（P. acnes）interacts with the SGs. We explored the effects of P. acnes and peptidoglycan (PGN) on the aryl hydrocarbon receptor (AhR) activation, lipogenesis and differentiation in cultured human SZ95 sebocytes in vitro. Both formaldehyde-inactivated P. acnes and PGN upregulated mRNA levels of AhR charachteristic downstream genes CYP1A1, CYP1B1, CYP1A2, as well as significantly induced translocation of AhR protein from cytoplasm into nucleus. GSEA revealed pathways of downregulated lipogenesis and upregulated keratinization. In addition, P.acnes and PGN inhibited linoleic acid(LA)-induced neutral lipid synthesis and expressions of Keratin 7 and Mucin1/EMA (sebocyte markers) and increased the expression of Keratin 10 and involucrin (keratinocyte markers), which were abolished after AhR gene silencing. Moreover, inhibited expressions of lipogenesis-related genes such as SREBP1 were observed. In conclusion, we provide evidence that P. acnes can switch sebocytes into a keratinocyte-like differentiation with reduced lipogenesis via AhR, indicating that follicular P. acnes should not only be considered as acnegenic but also as a factor promoting acne remission through feedback regulation of sebum production.
2019-07-16 | GSE134259 | GEO
Project description:The composition of the prostate microbiome may influence the fate of the cells that may be relevant to prostate morbidity. Several independent studies have reported the presence of the bacterium Propionibacterium acnes in diseased human prostate tissue. It is unclear if the bacterium is an infectious agent, part of a normal prostate microbiota or if it is derived from the skin and accidentally introduced, for instance during a prostate biopsy. Previous research with prostate cell culture and animal models has revealed the capability of P. acnes to establish a low-grade chronic inflammation. However, the fate of primary prostate cells exposed to P. acnes has not been investigated in molecular detail. Here, we investigated the impact of P. acnes on human primary prostate epithelial cells (PrEC). An initial analysis of the host cell response by microarray technology confirmed the inflammation-inducing capability of P. acnes but also showed the deregulation of genes involved in cell cycle, and more specifically in kinetochore and centromere functionality. In particular, we could show and confirm by qPCR that only viable P. acnes downregulated a master regulator of cell cycle progression, FOXM1, as well as its target genes. It was further shown by flow cytometry that P. acnes was indeed able to alter the cell cycle by increasing the number of PrEC cells in S-phase. In search for a molecular explanation we tested the hypothesis that a P.acnes produced berninamycin A-like thiopeptide, that is a structurally closely related to the known FOXM1 inhibitor siomycin A, is responsible for the effect on FOXM1 and the cell cycle. A knock-out mutant in P. acnes was created that lacked the gene encoding the berninamycin A peptide precursor; this mutant was unable to downregulate FOXM1, suggesting that a berninamycin A-like thiopeptide induces cell cycle alterations in PrEC cells. Interestingly, the gene cluster encoding this thiopeptide is restricted to a subtype of P. acnes that is relatively rare on human skin, but more often found in prostate tissue.
2016-07-11 | GSE72585 | GEO
Project description:Propionibacterium acnes HKGB1 Genome sequencing and assembly
| PRJNA636787 | ENA