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ABSTRACT: Periodontitis and neurodegenerative diseases

PROVIDER: PRJNA924699 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23097345_1.fastq.gz	Fastqsanger.gz
	SRR23097345_2.fastq.gz	Fastqsanger.gz
	SRR23097346_1.fastq.gz	Fastqsanger.gz
	SRR23097346_2.fastq.gz	Fastqsanger.gz
	SRR23097347_1.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:Common neuroinflammatory pathways in neurodegenerative diseases.

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RNA-seq analyses of periodontal tissue and liver of periodontitis-affected mice

Project description:Background/purpose Periodontal diseases exacerbate hepatic inflammation and diseases like non-alcoholic fatty liver disease via circulating pathogenic factors from periodontal tissue. Long-term pre-symptomatic state eventually leads to the development of such hepatic diseases. However, it is uncertain if periodontitis contributes in the onset of hepatic pre-symptomatic state. Herein, we conducted a hepatic whole transcription analysis of periodontitis-affected mice and healthy mice to understand the early functional changes in the hepatic system in periodontitis-affected mice. Materials and methods Silk ligatures were tied around mice second maxillary molars for 14 days to develop periodontitis. RNA-seq samples were collected from periodontal tissues and liver tissues of mice with periodontitis and healthy mice. Lipidomic analysis of hepatic omega-3 fatty acids in periodontitis-affected and healthy mice was conducted. The anti-inflammatory effects of omega-3 fatty acids and their metabolites were elucidated using hepatocytes HepG2 cells. Results In the liver of mice with periodontitis, genes coding for cytochrome P450 such as Cyp4a12a and Cyp4a12b were identified as significantly down-regulated genes. Lipidomic analyses identified that epoxidation and subsequent hydrolysis of hepatic omega-3 fatty acids were inhibited in periodontitis-affected mice. Eicosapentaenoic acid metabolites, epoxy eicosatetraenoic acid and dihydroxyeicosatetraenoic acid, inhibited inflammatory responses of HepG2 cells. Conclusion These results suggest that, in the liver of periodontitis-affected mice, due to the reduced activity of omega-3 fatty acid epoxidation, pre-symptomatic state with pro-inflammatory status develop. Therefore, early intervention of periodontitis might contribute to the prevention of the onset of hepatic diseases.

2024-05-03 | GSE264546 | GEO

peripheral blood mononuclear cells (PBMCs) of pre- and post-treatment periodontitis patients and healthy donors by single-cell RNA profiling

Project description:The pathogenic determinants of chronic periodontitis leading to extra-oral comorbidity are unclear. This study was conducted to investigate the main determinants that correlate chronic periodontitis and systemic diseases via periodontitis-evoked molecular changes in immune cells resolved by therapy. Single-cell RNA sequencing using peripheral blood mononuclear cells was performed to compare the molecular and biological differences in immune cells of 4 pre- and 4 post-treatment patients and 4 healthy donors. Periodontal treatment was one-day full-arch scaling and root planning for full mouth disinfection. Altered expression of genes involved in the inflammatory response in the patients was compared with that in healthy donors following therapeutic intervention. The common representative genes across diverse cell types were investigated; those genes were associated with periodontitis-pathogenic bacterial systemic diseases. These important factors correlating chronic periodontitis and systemic inflammatory diseases at the single-cell level may serve as therapeutic targets.

2022-11-09 | GSE174609 | GEO

Role of Microglia Somatic Mutations in Neurodegenerative Diseases

Project description:Role of Microglia Somatic Mutations in Neurodegenerative Diseases

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Role of Microglia Somatic Mutations in Neurodegenerative Diseases

Project description:Role of Microglia Somatic Mutations in Neurodegenerative Diseases

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Porphyromonas gingivalis triggers microglia activation and neurodegenerative processes through NOX4

Project description:Periodontitis and infections with periodontal bacteria have been highlighted as risk factors for dementia. In recent years attention has been drawn to the role of microglia cells in neurodegenerative diseases. However, there is limited knowledge of the influence of periodontal bacteria on microglia cells. The aim of the present study was to investigate the interactions between the periodontal bacteria P. gingivalis and microglia cells, and to unravel if these interactions could contribute to Alzheimer’s pathology. Periodontitis and infections with periodontal bacteria have been highlighted as risk factors for dementia. In recent years attention has been drawn to the role of microglia cells in neurodegenerative diseases. However, there is limited knowledge of the influence of periodontal bacteria on microglia cells. The aim of the present study was to investigate the interactions between the periodontal bacteria P. gingivalis and microglia cells, and to unravel if these interactions could contribute to Alzheimer’s pathology. We found, through microarray analysis, that stimulation of microglia cells with P. gingivalis resulted in upregulation of several Alzheimer´s disease associated genes, including NOX4. We also showed that P. gingivalis LPS mediated ROS production and IL-6 and IL-8 induction via NOX4 in microglia. The viability of neurons was shown to be reduced by conditioned media from microglia cells stimulated with P. gingivalis LPS, and that the reduction was NOX4 dependent. The levels of total and phosphorylated Tau in neurons were increased by conditioned media from microglia cells stimulated with P. gingivalis or LPS. This increase was NOX4 dependent. In summary our findings give us a potential mechanistic explanation of how the periodontal pathogen P. gingivalis could trigger or exacerbate AD pathogenesis.

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Mus musculus

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Project description:Saccharibacteria (TM7) are obligate epibionts living on the surface of their host bacteria, and strongly correlated with dysbiotic microbiomes during periodontitis and other inflammatory diseases, suggesting they are putative pathogens. However, due to the recalcitrance of TM7 cultivation, no causal research has been conducted to investigate their role in inflammatory diseases. Here, we isolated multiple TM7 species on their host bacteria from periodontitis patients. These TM7 species reduced inflammation and consequential bone loss by modulating their host bacterial pathogenicity in mouse ligature-induced periodontitis model. Two host bacterial functions involved in collagen binding and utilization of eukaryotic sialic acid were identified as required for inducing bone loss and altered by TM7 association. This down-regulation of host bacterial pathogenicity by TM7 was shown for multiple TM7/host bacteria pairs, suggesting that, in contrast to their suspected pathogenic role, TM7 could protect mammalian hosts from inflammatory damage induced by their host bacteria.

2023-03-11 | PXD026999 | Pride

Somatic mutations in Single Human Neurons from Patients with Congenital Neurodegenerative Diseases

Project description:Somatic mutations in Single Human Neurons from Patients with Congenital Neurodegenerative Diseases

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Somatic mutations in Single Human Neurons from Patients with Congenital Neurodegenerative Diseases

Project description:Somatic mutations in Single Human Neurons from Patients with Congenital Neurodegenerative Diseases

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