Explore the gene expression files of HGECs after P. gingivalis persisters treatment via RNA sequencing
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA766231 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16071415_1.fastq.gz | Fastqsanger.gz | |||
| SRR16071415_2.fastq.gz | Fastqsanger.gz | |||
| SRR16071416_1.fastq.gz | Fastqsanger.gz | |||
| SRR16071416_2.fastq.gz | Fastqsanger.gz | |||
| SRR16071417_1.fastq.gz | Fastqsanger.gz |
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Project description:This study investigated how P. gingivalis persisters interacted with human gingival epithelial cells (HGECs) and affected the gene expression of cytokines, and the related signaling pathways, via RNA sequencing. P. gingivalis (ATCC 33277) was treated with metronidazole (100 μg/ml) for 6 hours to generate P. gingivalis persisters (M-PgPs). HGECs with or without IL-1β pretreatment were stimulated by M-PgPs and P. gingivalis for 24 hours, and those without any treatments served as the blank control (BL).
2022-05-31 | GSE184777 | GEO
Project description:This project investigated the phenotypic characteristics of Metronidazole-tolerant Porphyromonas gingivalis persisters, the relevant modulatory effects of hemin and their underlying survival mechanisms. Proteomic analysis was performed to delineate the protein expression profiles of Metronidazole-tolerant P. gingivalis persister fractions and the controls incubated with different levels of hemin supplementation.
2018-08-29 | PXD008976 | Pride
Project description:Many bacterial infections are hard to treat and tend to relapse, possibly due to the presence of antibiotic-tolerant persisters that are considered dormant cells when bacteria are grown in laboratory medium. Non-growing persisters also form following uptake of Salmonella by macrophages but their nature is little understood. Here we show that Salmonella persisters arising during macrophage infection maintain an active state. Persisters reprogram macrophages by means of effectors secreted by the SPI-2 Type 3 Secretion System (T3SS), thereby dampening pro-inflammatory innate immune responses and inducing anti-inflammatory macrophage polarisation. Reprogramming allows non-growing Salmonella to survive for extended periods in their host. Persisters undermining the host immune defences might confer an advantage to the pathogen during relapse once the antibiotic pressure is relieved.
2018-12-07 | GSE104785 | GEO
Project description:Bacterial persister cells are phenotypic variants that exhibit a transient non-growing state and antibiotic tolerance. Here we provide in vitro evidence of Staphylococcus aureus persisters within infected host cells. We show that the bacteria surviving antibiotic treatment within host cells are persisters, displaying biphasic killing and reaching a uniformly non-responsive, non-dividing state when followed at the single-cell level. This phenotype is stable but reversible upon antibiotic removal. Intracellular S. aureus persisters remain metabolically active, but display an altered transcriptomic profile consistent with activation of stress responses, including the stringent response as well as cell-wall stress, SOS and heat-shock responses. These changes are associated with multidrug tolerance after exposure to a single antibiotic. We hypothesize that intracellular S. aureus persisters may constitute a reservoir for relapsing infection, and could contribute to therapeutic failures.
2020-03-25 | GSE139659 | GEO
Project description:Recent epidemiological studies revealed a significant association between oral squamous cell carcinoma (OSCC) and Porphyromonas gingivalis, a major pathogen of periodontal disease. As a keystone pathogen, P. gingivalis is known not only to damage local periodontal tissue, but also to evade from the host immune system and eventually affect systemic health. However, its role in OSCC has yet to be well studied. To explore the underlying effect of chronic P. gingivalis infection on OSCC and to identify relevant biomarkers as promising targets for therapy and prevention, we established a novel model by exposing human immortalized oral epithelial cells (HIOECs) to P. gingivalis at a low MOI for 5 to 23 weeks. The P. gingivalis-infected HIOECs were monitored in tumor biological alteration. Bioinformatics analyses were performed on HIOECs infected for 15 weeks, and some selected data were validated by q-PCR and (or) Western blot on cells infected for 15 and 23 weeks. Accordingly, we found that persistent exposure to P. gingivalis induced tumor biological properties on HIOECs. Tumor-related genes such as NNMT, FLI1, GAS6, lncRNA CCAT1, PDCD1LG2 and CD274 were aberrantly expressed in response to long-term exposure of P. gingivalis. In addition, some clinical biomarkers and novel proteins were presented. In conclusion, chronic P. gingivalis infection may be a potential risk factor of OSCC. The key regulators and biomarkers might be used in monitoring OSCC with chronic periodontal infection. We applied lncRNA Microarray (Affymetrix) which could simultaneously detect coding and non-coding genes to explore the differences of cell gene expression after long-term exposure to P. gingivalis.
2017-06-01 | GSE87539 | GEO
Project description:The outer membrane vesicles (OMVs) produced by Porphyromonas gingivalis (P. gingivalis) contain a variety of bioactive molecules that may be involved in the progression of periodontitis. However, the participation of P. gingivalis OMVs in the development of periodontitis has not been elucidated. Here we isolated P. gingivalis OMVs and confirmed their participation in periodontitis both in vivo and in vitro. Microcomputed Tomography (micro-CT) and histological analysis showed that under the stimulation of P. gingivalis OMVs, the alveolar bone of rats was significantly resorbed in vivo. We found that P. gingivalis OMVs were taken up by hPDLCs (human Periodontal Ligament Cells, hPDLCs) in vitro, then subsequently resulting in apoptosis and inflammatory cytokines releasing which was accomplished by the microRNA-size small RNAs (msRNAs) sRNA45033 in the P. gingivalis OMVs. Through bioinformatics analysis and screening of target genes, Chromobox 5 (CBX5) was identified as the downstream target of screened-out small RNA s45033. Using dual-luciferase reporter assay, overexpression, and knockdown methods, s45033 was confirmed to target CBX5 to regulate hPDLCs apoptosis. In addition, Cleavage Under Targets and Tagmentation (Cut&Tag) analysis confirmed the mechanism that CBX5 regulates apoptosis through the methylation of p53 DNA. Collectively, these findings indicate that the role of P. gingivalis OMVs is immunologically relevant and related to bacterial virulence in the development of periodontitis.
2022-11-30 | GSE218606 | GEO
Project description:Purpose: To investigate the pathogenic effect of P. gingivalis on normal esophagus and the mechanism behind Methods: Total mRNA was extracted to determine the transcriptional dysregulation of Het-1A cells after treated with P. gingivalis supernatant.
2022-09-18 | GSE210408 | GEO
Project description:Proteomics is the most suitable tool to study persisters with their complex underlying molecular mechanisms from a system-level perspective, but the number of persisters that present naturally is too few for proteomics analysis. Here, we utilized Evo3A, an evolved population with enriched persisters fraction from a recent adaptive laboratory evolution experiment, to study the mechanisms of persistence during ampicillin treatment and resuscitation. Interestingly, the enriched persisters on Evo3A exhibit filamentous morphology upon treatment with ampicillin, and the filaments are getting longer over time. Time-course proteomics study revealed that proteins involved in major carbohydrate metabolism are up-regulated, in particular those involved in the oxidative stress response and act as cellular response to DNA damage. As opposed to the proteome profile during antibiotic treatment, proteins involved in major metabolic processes and ATP generation are down-regulated, while translational proteins and porins are up-regulated in the filaments during resuscitation.
2020-07-13 | PXD016271 | Pride
Project description:Non-genetic mechanisms have recently emerged as important drivers of therapy failure in cancer, where some cancer cells can enter a reversible drug-tolerant persister state in response to treatment. While most cancer persisters, like their bacterial counterparts, remain arrested in the presence of drug, a rare subset of cancer persisters can re-enter the cell cycle under constitutive drug treatment. Little is known about the non-genetic mechanisms that enable cancer persisters to simultaneously resist therapy and maintain proliferative capacity in the presence of drug. To address this, we developed Watermelon, a new high-complexity expressed barcode lentiviral library for simultaneous tracing each cell's clonal origin, proliferative state, and transcriptional state, and used it to study this rare, transiently-resistant, proliferative persister population and identify what distinguishes it from non-cycling persisters. Analysis of Watermelon-transduced cancer cell lines demonstrated that cycling and non-cycling persisters arise from different pre-existing cell lineages with distinct transcriptional and metabolic programs. The proliferative capacity of persisters is associated with an upregulation of antioxidant gene programs and a metabolic shift to fatty acid oxidation in specific subpopulations of tumor cells.
2020-05-21 | GSE150949 | GEO