Oral bacterial dysbiosis drives autoimmune heart disease via molecular mimicry
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE310386 | GEO | 2025/11/24
REPOSITORIES: GEO
Similar Datasets
Project description:Oral bacterial dysbiosis drives autoimmune heart disease via molecular mimicry
| PRJNA1365864 | ENA
Project description:The goal of this study was to compare the gene expression profiles of chronically inflamed human peri-implant and chronically inflamed human periodontal tissues in order to elucidate potential changes at the molecular level. Cells out of the pocket depth of the inflamed peri-implant and periodontal ligament as well as from the middle third of healthy periodontal ligament were applied. Genome-wide gene expression was compared with the help of microarray analysis, and the data were validated by real-time RT-PCR. The expression rates of 14,239 genes were investigated and 2,079 of them were found differentially expressed by at least two-fold; the expression rates of 1,093 genes were significantly up-regulated and the expression rates of 986 genes were significantly down-regulated in inflamed peri-implant cells compared to inflamed periodontal cells. We focused on genes coding for extracellular matrix components and those that degrade them. Only genes of non-fibril-forming collagens (types IV, VI, VII, and XVII) were increased in inflamed peri-implant tissue, whereas only the genes of two fibril-forming collagens (types III and XVII) were decreased, suggesting that peri-implant tissue re-models faster than periodontal tissue. Furthermore, cathepsin D and cathepsin S might participate to a greater extent in connective tissue destruction of peri-implant tissue. The present investigation demonstrated that, despite their clinical similarities, periimplantitis and periodontitis are two different diseases at the genetic level. Keywords: inflammation, peri-implant, periodontal ligament cells The peri-implant tissue was scraped of the implant and the periodontal tissue was scraped off the roots of the teeth. Both tissue probes were treated with the RNeasy mini Kit (Qiagen, Hilden, Germany) to isolate total RNA from chronically inflamed peri-implant and chronically inflamed PDL cells, according to the manufacturer’s instructions. Healthy PDL cells were taken from the middle third of the root clearly avoiding sampling the gingiva. The chronically inflamed peri-implant and periodontal cells were taken directly out of the depth of the pocket again avoiding the ingrown gingiva. Quality control and quantitation of total RNA samples were determined prior to the microarray experiments (Agilent 2100 Bioanalyzer, Agilent Technologies, Palo Alto, CA, USA). Equal amounts of total RNA were pooled into an inflamed peri-implant and an inflamed and healthy periodontal cell pool. To monitor the relative abundance of mRNA for full-length human genes, the Affymetrix GeneChip HG_U133A was used, representing 22,283 probe sets (14,239 unique human genes). Labelled cRNA, fragmented to an average size of 100–150 bases, was hybridized to the GeneChips. For each pool of cRNA, two GeneChips were hybridized. Chronically inflamed peri-implant as well as healthy and chronically inflamed periodontal tissue was collected from 48 patients at the Dental Medical School of the University of Goettingen (21 men, 27 women, aged between 18 and 72 years) from March 2005 to August 2006, as already described by Gersdorff et al. (2007). The peri-implant tissue probes were taken from endosteal implants (Astra Tech®, ITI Bonefit®, or Brånemark®) with chronic peri-implant lesions (Schwarz et al. 2007). The periodontal tissue probes were taken from teeth, either extracted for orthodontic reasons or due to carious lesions (healthy periodontium) or from teeth with generalized chronic periodontitis (Armitage 2004). Teeth with healthy PDL had no clinical signs of inflammation (no bleeding on probing), exhibited a probing depth of ?3,5 mm and had no radiographic detectable bone loss. In contrast, implants and teeth with generalized chronic inflammation exhibited obvious clinical signals of inflammation (bleeding on probing), exhibited a probing depth of >4 mm and had radiographic evidence of bone loss (1 to 7 mm). A detailed anamnesis of each patient was explored. All patients were without a medical history, i.e. heart diseases or diabetes, and were not on medication. In addition, the tissue samples used in our study were only taken from non-smokers. The explanted implants and extracted teeth were immediately frozen and stored at -80 °C. All patients who participated in the study were informed about the nature and aim of this project and gave their written informed consent. The study was approved according to the regulations of the Ethics Committee of the Medical Faculty of the University of Goettingen.
2009-08-30 | E-GEOD-8908 | biostudies-arrayexpress
Project description:The periodontium are the tissues supporting and investing the tooth and consists of the periodontal ligament, the gingiva, the root cementum, and the alveolar bone. The functions of the cell populations in health and disease regarding the host-mediated tissue destruction are not well understood. To get a first idea, of which genes might play a distinct role in chronic periodontal disease in vivo, we compared the genom-wide gene expressions of chronic inflamed and healthy periodontal ligament cells by microarray analysis and validated the data by real-time RT-PCR. The expression rates of 14.239 genes were investigated and 3.018 of them were found differentially expressed by at least two-fold, the expression rates of 1.451 genes were significantly up-regulated and the expression rates of 1.567 genes were significantly down-regulated in inflamed PDL cells. We focused on mainly structural components, for example, laminins and integrins, as well as degrading enzymes, for example, MMPs and cathepsins. The molecular composition of the laminin network varies in chronic inflamed compared to healthy PDL cells in vivo. Furthermore, integrin alpha6beta4, together with laminin-332, might be involved in chronic periodontal inflammation. Findings that diverse keratins were upregulated in chronic disease indicate that the epithelial cell rests of Malassez might also be involved in chronic periodontal inflammation. Also cathepsin B and cathepsin C might participate in the connective tissue destruction. The microarray analysis has identified a profile of genes potentially involved in chronic periodontal inflammation in vivo. Further studies are needed to entirely understand cellular activities during chronic periodontal inflammation in vivo. Keywords: expression analysis
2007-08-01 | GSE7321 | GEO
Project description:The periodontium are the tissues supporting and investing the tooth and consists of the periodontal ligament, the gingiva, the root cementum, and the alveolar bone. The functions of the cell populations in health and disease regarding the host-mediated tissue destruction are not well understood. To get a first idea, of which genes might play a distinct role in chronic periodontal disease in vivo, we compared the genom-wide gene expressions of chronic inflamed and healthy periodontal ligament cells by microarray analysis and validated the data by real-time RT-PCR. The expression rates of 14.239 genes were investigated and 3.018 of them were found differentially expressed by at least two-fold, the expression rates of 1.451 genes were significantly up-regulated and the expression rates of 1.567 genes were significantly down-regulated in inflamed PDL cells. We focused on mainly structural components, for example, laminins and integrins, as well as degrading enzymes, for example, MMPs and cathepsins. The molecular composition of the laminin network varies in chronic inflamed compared to healthy PDL cells in vivo. Furthermore, integrin alpha6beta4, together with laminin-332, might be involved in chronic periodontal inflammation. Findings that diverse keratins were upregulated in chronic disease indicate that the epithelial cell rests of Malassez might also be involved in chronic periodontal inflammation. Also cathepsin B and cathepsin C might participate in the connective tissue destruction. The microarray analysis has identified a profile of genes potentially involved in chronic periodontal inflammation in vivo. Further studies are needed to entirely understand cellular activities during chronic periodontal inflammation in vivo. Experiment Overall Design: Periodontal tissue was collected from 32 patients at the Dental Medical School of the University of Goettingen (12 men, 20 women, aged between 18 and 72 years) from March 2005 to Dezember 2005. The tissue probes were taken from teeth, either extracted for orthodontic reasons (healthy periodontium) or because of chronic periodontal lesions. The differentiation between both collectives was performed using clinical and radiological parameters (clinical attachment loss, increase in probing depth, and radiographic bone loss). A detailed anamnesis of each patient was explored. All patients were without a medical history and were not on medication. In addition, the tissue samples used in our study were only taken from non-smokers. The extracted teeth were immediately frozen and stored at -80°C. All patients who participated in the study were informed about the nature and aim of this project and gave their written informed consent. The study was approved according to the regulations of the Ethics Committee of the Medical Faculty of the University of Goettingen.
2008-06-15 | E-GEOD-7321 | biostudies-arrayexpress
Project description:Peri-implantitis is a common complication characterized by chronic inflammation of the periodontal tissue. This disease is marked by irreversible and progressive degradation of the gingiva and alveolar bone, ultimately leading to tooth loss.Most current research has focused on the entire periodontal tissue, which restricts a comprehensive understanding of the heterogeneity between gingiva and bone tissues, and hinders the development of targeted host therapies for peri-implantitis. To uncover the pathogenic mechanisms of peri-implantitis, our study employed a tissue-specific approach to investigate the interactions between stromal and immune cells in gingiva and bone tissues separately, using single-cell sequencing techniques. This strategy aims to develop the insights of the pathogenesis of peri-implantitis, providing a scientific basis for the treatment of peri-implantitis.
2024-11-11 | GSE281266 | GEO
Project description:The oral gingival barrier is a constantly stimulated and dynamic environment where homeostasis is often disrupted, resulting in inflammatory periodontal diseases. Type 2 diabetes (T2D), a risk factor for periodontitis, has been reported to be associated with barrier dysfunction, but the effect and underlying mechanism are inconclusive. Herein, we performed single-cell RNA sequencing (scRNA-seq) of gingiva from leptin receptor-deficient (db/db) mice to understand the heterogeneity of gingival barrier in the context of T2D. Periodontal health of control mice is characterized by populations of Krt14+-expressing epithelial cells and Col1a1+-fibroblasts mediating immune homeostasis primarily through the enrichment of innate lymphoid cells. The db/db mice exhibit an impaired gingival barrier with spontaneous periodontal bone loss, and a decreased proportion of epithelial/stromal cells. We further observed stromal, particularly fibroblast immune hyperresponsiveness linked to recruitment of myeloid cell populations in gingiva from T2D mice. Analysis of ligand-receptor interaction pairs suggested inflammatory signaling between fibroblasts and myeloid cells, a main driver of diabetes-induced periodontal damage. Moreover, the “Immune-like” stromal cells contributed to gingival Th17/IL-17 hyperresponsiveness in T2D. Our work reveals transcriptional diversity of stromal cells and interaction with innate immune cells in T2D, and uncovers the “immune-like” fibroblast subsets participating in barrier homeostasis at the diabetic gingiva.
2022-01-01 | GSE188217 | GEO
Project description:The goal of this study was to compare the gene expression profiles of chronically inflamed human peri-implant and chronically inflamed human periodontal tissues in order to elucidate potential changes at the molecular level. Cells out of the pocket depth of the inflamed peri-implant and periodontal ligament as well as from the middle third of healthy periodontal ligament were applied. Genome-wide gene expression was compared with the help of microarray analysis, and the data were validated by real-time RT-PCR. The expression rates of 14,239 genes were investigated and 2,079 of them were found differentially expressed by at least two-fold; the expression rates of 1,093 genes were significantly up-regulated and the expression rates of 986 genes were significantly down-regulated in inflamed peri-implant cells compared to inflamed periodontal cells. We focused on genes coding for extracellular matrix components and those that degrade them. Only genes of non-fibril-forming collagens (types IV, VI, VII, and XVII) were increased in inflamed peri-implant tissue, whereas only the genes of two fibril-forming collagens (types III and XVII) were decreased, suggesting that peri-implant tissue re-models faster than periodontal tissue. Furthermore, cathepsin D and cathepsin S might participate to a greater extent in connective tissue destruction of peri-implant tissue. The present investigation demonstrated that, despite their clinical similarities, periimplantitis and periodontitis are two different diseases at the genetic level. Keywords: inflammation, peri-implant, periodontal ligament cells
2009-08-30 | GSE8908 | GEO
Project description:Mouse and human periodontal transcriptome (gingiva and microbiome)
| PRJNA950601 | ENA
Project description:Treatment of mouse skin with the staphylococcal protease SspA and house dust mite extract (HDM) results in dermatitis. Using a 10x Genomics Xenium In Situ platform, we analyzed spatial features in mock-treated skin and inflamed skin treated with epicutaneous SspA and HDM.
2025-11-24 | GSE310658 | GEO
Project description:Fusobacterium polymorphum isolate:Inflamed gingiva Genome sequencing and assembly
| PRJNA1051802 | ENA