Ontology highlight
ABSTRACT:
PROVIDER: PRJNA429201 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6451880.fastq.gz | Fastqsanger.gz | |||
| SRR6451890.fastq.gz | Fastqsanger.gz | |||
| SRR6451900.fastq.gz | Fastqsanger.gz | |||
| SRR6451910.fastq.gz | Fastqsanger.gz | |||
| SRR6451920.fastq.gz | Fastqsanger.gz |
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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.
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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:<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>
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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).
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Project description:The composition of the salivary microbiota has been reported to differentiate between patients with periodontitis, dental caries and orally healthy individuals. Thus, the purpose of the present investigation was to compare metaproteomic profiles of saliva in oral health and disease. Stimulated saliva samples were collected from 10 patients with periodontitis, 10 patients with dental caries and 10 orally healthy individuals. Samples were analyzed by means of shotgun proteomics. 4161 different proteins were recorded out of which 1946 and 2090 were of bacterial and human origin respectively. The human proteomic profile displayed significant overexpression of the complement system and inflammatory mediators in periodontitis and dental caries. Bacterial proteomic profiles and functional annotation were very similar in health and disease. Data revealed multiple potential salivary proteomic biomarkers of oral disease. In addition, comparable bacterial functional profiles were observed in periodontitis, dental caries and oral health, which suggest that the salivary microbiota predominantly thrives in a planktonic state expressing no characteristic disease-associated metabolic activity. Future large-scale longitudinal studies are warranted to reveal the full potential of proteomic analysis of saliva as a biomarker of oral health and disease.
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