Ontology highlight
ABSTRACT:
PROVIDER: PRJNA670573 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12875200_1.fastq.gz | Fastqsanger.gz | |||
| SRR12875200_2.fastq.gz | Fastqsanger.gz | |||
| SRR12875300_1.fastq.gz | Fastqsanger.gz | |||
| SRR12875300_2.fastq.gz | Fastqsanger.gz | |||
| SRR12875201_1.fastq.gz | Fastqsanger.gz |
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Project description:Korean oral microbiome across different periodontal health
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Project description:This study compared the subgingival microbiota of subjects with periodontitis to those with periodontal health using the Human Oral Microbe Identification Microarray (HOMIM).
2011-09-17 | GSE32159 | GEO
Project description:Objectives: Arterial hypertension (AH) influences salivary gland physiology and oral health, being associated with a higher incidence of periodontal disease in pregnant women. Evidence points to a bidirectional relationship between the oral microbiota and blood pressure regulation. Therefore, this study aimed to characterize the oral health of pregnant women and AH-associated changes in the salivary proteome and microbiome during pregnancy and postpartum. Design: Ten healthy women and ten women with AH were enrolled. Saliva was collected during pregnancy and six months postpartum. The salivary proteome was characterized by shotgun label-free mass spectrometry analysis. Specific proteins were validated through parallel reaction monitoring (PRM). The oral microbiota was characterized via 16S rRNA gene amplicon sequencing (V4 region). The periodontal health and the caries history was assessed during pregnancy. Results: Pregnant women with AH had lower junction plakoglobin (JUP)- and desmoplakin (DSP)-specific peptide levels than healthy women, confirmed by the PRM approach. The levels of these proteins correlated negatively with periodontal health indexes, which were higher in pregnant women with AH. In AH, nitrate-reducing microorganisms had lower abundance, correlating positively with JUP and DSP-specific peptides. Conclusions: The salivary proteome and microbiota are shaped by AH during and after pregnancy. Further research is required to understand the underlying mechanisms impairing oral health in AH. Data acquisition has been supported by EPIC-XS, project number 393, funded by the Horizon 2020 program of the European Union and the National Institute for Neurological Research (Programme EXCELES, ID Project No. LX22NPO5107) and the MEYS/EU project OP JAK-MULTIOMICS_CZ - Multi-omics platform for the search for biological correlates of diseases and the development of new diagnostic, preventive and therapeutic procedures (CZ.02.01.01/00/23_020/0008540).
2025-12-03 | PXD071471 | Pride
Project description:Periodontal health, disease, and reoslution are characterized by a diverse cellular immune response in the oral mucosa. We used scRNAseq to robustly characterize the imme cell repertoire and asosciated changes across changes of conditions of health and disease.
2024-08-22 | GSE244633 | GEO
Project description:The link between poor oral health and heart failure progression has long been recognized but remains limited to epidemiological associations without mechanistic understanding. Here, we performed Xenium in situ on heart tissue post-transplantation to detect CD4 T-cells that generated in inflamed gingiva during periodontal diseases.
2025-11-24 | GSE310386 | GEO
Project description:Background: Schizophrenia (SZ) is a chronic, severe mental disorder that presents significant challenges to diagnosis and effective treatment. Emerging evidence suggests that gut microbiota may play a role in the disease's pathogenesis. However, fewer studies have directly investigated the potential links between oral microbiota and SZ. Purpose: This study aimed to explore the relationship between salivary microbiota dysbiosis and SZ, examining microbial and metabolic alterations that may contribute to SZ pathophysiology. Methods: Salivary samples from 30 hospitalized patients diagosed with SZ and 10 healthy controls were collected. The microbial and metabolic profiles were analyzed using 16S rRNA gene sequencing and metabolomic profiling. Clinical parameters, including oral health status, were also evaluated to minimize variability in sampling. Results: Patients with SZ exhibited significantly poorer oral health compared to healthy controls, with more missing teeth and worse periodontal status. Microbiota sequencing revealed notable alterations in the overall structure and composition of the salivary microbiome in SZ patients, characterized by increased abundance of specific genera such as Neisseria and Porphyromonas. Metabolomic analysis indicated significant differences between the SZ and control groups, with upregulation of key metabolic pathways, including “β-alanine metabolism” and “vitamin digestion and absorption”. Correlations between microbial dysbiosis and elevated levels of certain metabolites, such as L-methionine sulfoxide (L-MetO) and tyramine, were observed, suggesting links to oxidative stress. Conclusion: The study highlights the presence of significant dysbiosis and metabolic dysfunction in the salivary microbiota of SZ patients, suggesting that alterations in the oral microbiome may contribute to SZ pathogenesis. These results provide new insights into potential diagnostic biomarkers and therapeutic targets for SZ. Further studies with larger sample sizes are required to validate these findings.
2025-11-27 | GSE283329 | GEO
Project description:The global high prevalence of COVID-19 is a major challenge for health professionals and patients. SARS-CoV-2 virus has four kinds of structural protein components: the spike protein, envelope protein, membrane protein, and nucleocapsid protein. SARS-CoV-2 virus mutate predominantly in the spike proteins, whilst the other key viral components remain stable. Essentially the pathological functions of the SARS-CoV-2 virus on different cell types are still largely unknown. Previous studies have shown that the human oral cavity can potentially act as reservoir of the SARS-CoV-2 virus. However, the consequence of SARS-CoV-2 viral infection on human oral health has not been systematically examined. COVID-19 can cause severe oral mucosa lesions and is likely to be connected with poor periodontal conditions. Fibroblasts are the key component of periodontal ligament (PDL) and express the SARS-CoV-2 receptor: Angiotensin-converting enzyme 2 (ACE2), whose expression level can increase upon bacterial infection hence potentially provide a direct route of SARS-CoV-2 infection to PDL fibroblasts. In this research, we aimed to study the pathogenicity of SARS-CoV-2 viral components on human fibroblasts. We found that by exposing to SARS-CoV-2, especially to the viral envelope and membrane proteins, the human periodontal fibroblasts could develop fibrotic pathogenic phenotypes, including hyperproliferation that was concomitant induced together with increased apoptosis and senescence. The fibrotic degeneration was mediated by a down-regulation of mitochondrial -oxidation in the fibroblasts. Fatty acid -oxidation inhibitor, etomoxir treatment could mirror the same pathological consequence on the cells, similar to SARS-CoV-2 infection. Our results therefore provide novel mechanistic insights into how SARS-CoV-2 infection can affect human periodontal health at the cell and molecular level with potential new therapeutic targets for COVID-19 induced fibrosis.
2023-07-20 | PXD041281 | Pride
Project description:<h4><strong>BACKGROUND AND HYPOTHESIS: </strong>It is presently unclear why there is a high prevalence of periodontal disease in individuals living with chronic kidney disease. Whilst some have argued that periodontal disease causes chronic kidney disease, we hypothesized that alterations in saliva and the oral microenvironment in organisms with kidney disease may initiate periodontal disease by causing dysbiosis of the oral microbiota.</h4><h4><strong>METHODS: </strong>Experimental kidney disease was created using adenine feeding and subtotal nephrectomy in rats, and by adenine feeding in mice. Loss of periodontal bone height was assessed using a dissecting microscope supported by micro-CT, light, confocal and electron microscopy, and immunohistochemistry. Salivary biochemistry was assessed using NMR spectroscopy. The oral microbiome was evaluated using culture-based and molecular methods, and the transmissibility of dysbiosis was assessed using co-caging and microbial transfer experiments into previously germ-free recipient mice.</h4><h4><strong>RESULTS: </strong>We demonstrate that experimental kidney disease causes a reproducible reduction of alveolar bone height, without gingival inflammation or overt hyperparathyroidism but with evidence of failure of bone formation at the periodontal crest. We show that kidney disease alters the biochemical composition of saliva and induces progressive dysbiosis of the oral microbiota, with microbial samples from animals with kidney disease displaying reduced overall bacterial growth, increased alpha diversity, reduced abundance of key components of the healthy oral microbiota such as Streptococcus and Rothia, and an increase in minor taxa including those from gram-negative phyla Proteobacteria and Bacteroidetes. Co-housing diseased rats with healthy ones ameliorates the periodontal disease phenotype, whilst transfer of oral microbiota from mice with kidney disease causes periodontal disease in germ-free animals with normal kidney function.</h4><h4><strong>CONCLUSIONS: </strong>We advocate that periodontal disease should be regarded as a complication of kidney disease, initiated by oral dysbiosis through mechanisms independent of overt inflammation or hyperparathyroidism.</h4>
2025-09-04 | MTBLS1833 | MetaboLights