Ontology highlight
ABSTRACT:
PROVIDER: PRJNA648141 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12324500_1.fastq.gz | Fastqsanger.gz | |||
| SRR12324500_2.fastq.gz | Fastqsanger.gz | |||
| SRR12324600_1.fastq.gz | Fastqsanger.gz | |||
| SRR12324600_2.fastq.gz | Fastqsanger.gz | |||
| SRR12324501_1.fastq.gz | Fastqsanger.gz |
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Project description:Causes necrotizing periodontal disease
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Project description:Causes periodontal disease, gum inflamation
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Project description:Onset of chronic periodontitis is associated with an aberrant polymicrobial community, termed dysbiosis. Findings of a recent model of its etiology suggested that dysbiosis holds a conserved metabolic signature as an emergent property. The purpose of this study was to identify robust biomarkers for periodontal inflammation severity. Furthermore, we investigated disease-associated metabolic signatures of periodontal microbiota using a salivary metabolomics approach. Collection of whole saliva samples was performed before and after removal of supragingival plaque (debridement). Periodontal inflamed surface area (PISA) was employed as an indicator of periodontal inflammatory status. Based on multivariate analyses using pre-debridement salivary metabolomics data, we found that the metabolites associated with higher PISA included cadaverine and hydrocinnamate, while uric acid and ethanolamine were associated with lower PISA. Next, we focused on dental plaque metabolic byproducts by selecting significantly decreased salivary metabolites following debridement. Metabolite set enrichment analysis revealed that polyamine metabolism, arginine and proline metabolism, butyric acid metabolism, and lysine degradation were distinctive metabolic signatures of dental plaque in the high PISA group, which may have relevance to the metabolic signatures of disease-associated communities. Collectively, our findings identified potential biomarkers of periodontal inflammatory status, while they also provide insight into metabolic signatures of dysbiotic communities.
2016-10-23 | ST000496 | MetabolomicsWorkbench
Project description:Periodontitis is a chronic inflammatory disease resulting from a dysbiosis of the dental biofilm and a dysregulated host response in susceptible individuals. It is characterized by periodontal attachment destruction, bone resorption, and eventual tooth loss. Salivary biomarkers have been sought to predict and prevent periodontitis. This comparative study analyzed the salivary proteome of 30 individuals with chronic periodontitis (CP) and 10 with periodontal health (PH), and correlated specific proteins with clinical parameters of disease by using mass spectrometry. Stimulated whole saliva was obtained and pooled for 5 healthy controls and 15 CP patients, precipitated with TCA, digested enzymatically with trypsin and analyzed by an LTQ Orbitrap Velos equipped with a nanoelectrospray ion source. A wide range of salivary proteins of various functions was significantly reduced in CP individuals, whereas salivary acidic proline-rich phosphoprotein, submaxillary gland androgen-regulated protein, histatin, fatty acid-binding protein, thioredoxin, and cystatin were predominant in diseased patients and correlated significantly with signs of periodontal attachment loss and inflammation. Specific salivary proteins were associated with PH and CP. These differences in salivary proteome profiles may contribute to the identification of disease indicators or signatures and the improvement of periodontal diagnosis.
2020-05-20 | PXD015024 | Pride
Project description:Periodontal disease (PD) is characterized by inflammation affecting the tissue surrounding the teeth, primarily affecting the soft tissues, like the gingiva. However, without proper treatment, the condition exacerbates and progresses to impact the deeper structures, as the alveolar bone. The periodontal inflammation leads to the alveolar bone resorption, that eventually results in the complete loss of tooth support. Given its potential consequences, periodontal disease is a significant public health concern, as one of the primary causes of tooth loss, contributing to issues such as impaired mastication, speech difficulties, low self-esteem, and quality of life. Notably, comorbidities, like hypertension, can exacerbate the progression and severity of periodontal disease. In addition, the coexistence of periodontal disease and hypertension is highly likely to occur due to sharing of several risk factors. A better understanding of the underling molecular mechanisms associated to the severity of periodontal disease in the context of hypertension would greatly contribute to the advancement of translational research in the field of periodontics. MicroRNAs, a class of small non-coding RNA molecules, have an important role in regulating gene expression at the post-transcriptional level. These molecules can regulate multiple mRNA targets through complementary base pairing between the miRNA 5' seed sequence and the mRNA 3' untranslated region (UTR). Therefore, microRNAs can potentially modulate a wide variety of cellular processes, in both normal and pathological contexts. Presently, most of the studies in the field concentrate on the periodontium soft tissues, while our understanding of microRNA modulation in the alveolar bone remains comparatively limited. We used microarray analysis to evaluate the expression profiles of microRNAs in the mandibles of Wistar and SHR rats with periodontal disease, compared to their respective control groups. Our aim was to identify microRNAs of interest that could possibly be associated to the periodontal disease-induced alveolar bone loss.
2023-11-21 | GSE241787 | GEO
Project description:Morphine causes microbial dysbiosis. In this study we focused on restoration of native microbiota in morphine treated mice and looked at the extent of restoration and immunological consequences of this restoration. Fecal transplant has been successfully used clinically, especially for treating C. difficile infection2528. With our expanding knowledge of the central role of microbiome in maintenance of host immune homeostasis17, fecal transplant is gaining importance as a therapy for indications resulting from microbial dysbiosis. There is a major difference between fecal transplant being used for the treatment of C. difficile infection and the conditions described in our studies. The former strategy is based on the argument that microbial dysbiosis caused by disproportionate overgrowth of a pathobiont can be out-competed by re-introducing the missing flora by way of a normal microbiome transplant. This strategy is independent of host factors and systemic effects on the microbial composition. Here, we show that microbial dysbiosis caused due to morphine can be reversed by transplantation of microbiota from the placebo-treated animals.
2016-06-01 | E-MTAB-3723 | biostudies-arrayexpress
Project description:Objective Ulcerative colitis (UC) is a risk factor of periodontitis. This study aimed to investigate whether hematopoietic stem and progenitor cells (HSPCs) and their myeloid progeny exacerbate periodontal inflammation in UC. Design Ligature-induced periodontitis (LIP) was established in dextran sulfate sodium (DSS)-induced colitis (DIC) C57BL/6 mice. The bone resorption, intestinal and periodontal inflammation were evaluated by micro-CT and histological analyses. Inflammatory cytokines and lipopolysaccharide (LPS) in serum and gut microbiota were assessed by multiplexed flow cytometric assay, ELISA and 16S rRNA sequencing, respectively. Flow cytometry was performed to analyze HSPCs differentiation, and to sort hematopoietic stem cells for transcriptomic analysis. Berberine treatment of DIC was employed to investigate whether dampening of DIC would alleviate periodontitis. Results DIC mice exhibited disrupted intestinal barrier with dysbiotic gut microbiota, corroborating the elevated serum level of LPS and IL-1. Compared to DIC-free/LIP mice, DIC/LIP mice showed aggravated alveolar bone resorption, with enrichment of neutrophils extracellular traps (NETs) in periodontal tissues. DIC promoted myelopoiesis of HSPCs by up-regulating myeloid differentiation pathway. Intragastric administration of berberine dampened DIC and rescued the myeloid skewing of HSPCs, consequently alleviating periodontal destruction. Intriguingly, LIP induction after DIC remission still exhibited aggravated periodontal destruction and myeloid skewing of HSPCs, indicating a UC-trained immunity against periodontal infection. Conclusion Increased gut permeability and microbial dysbiosis in UC elevate the serum level of LPS and IL-1, inducing myeloid skewing of HSPCs with an immune memory. Generation of inflammatory potential myeloid cells causes NETs accumulation and aggravates periodontal destruction in the UC-related periodontitis.
2023-12-10 | GSE249582 | GEO