Oral microbiome
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ABSTRACT:
PROVIDER: PRJNA763064 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The aim of this study was to explore whether differences exist and to what an extent of the immune-mediated inflammatory reactions between periodontitis and peri-implantitis at the transcriptional level in the same susceptible host. Methods: Ligature-induced experimental peri-implantitis and periodontitis in the same mice were established. Gingival tissues of healthy, periodontitis and peri-implantitis sites from the same oral cavity were collected and used for RNA-sequencing. Differentially expressed genes (DEGs) were screened between periodontitis/peri-implantitis sites and healthy sites. The enrichment analysis of DEGs were analyzed. Comprehensive immune landscape was annotated by seq-ImmuCC. Results: The results showed that 137 and 353 up-regulated DEGs as well as and 670 and 174 down-regulated DEGs were specifically expressed periodontitis/peri-implantitis group compared to the healthy control group, respectively. The pathways of complement and coagulation cascade and osteoclast differentiation were dominating in the peri-implantitis sites. Moreover, peri-implantitis sites exhibited elevated macrophage proportions and relatively enriched macrophage activation and bone loss compared with periodontitis. Conclusions: Results indicated that peri-implantitis and periodontitis exhibited significantly distinct transcriptional signatures. Additionally, the study suggests that the interplay between macrophages and bone resorption are comparatively more active in peri-implantitis compared with periodontitis. These biological processes may be factors contributing to the pathogenesis of peri-implantitis being distinct from that of periodontitis.
2022-06-06 | GSE186882 | GEO
Project description:This study included 20 participants (10 healthy subjects and 10 patients with periodontitis and peri-implantitis). Gingival tissue samples (10 healthy, 10 periodontitis, and 10 peri-implantitis tissues) were collected, RNAs were extracted, and RNA sequencing and analysis were performed.
2024-01-29 | GSE223924 | GEO
Project description:Transcriptome analysis of oral tissue samples taken from peri-implantitis and healthy control patients Peri-implantitis is a condition resulting in destructive inflammation in the peri-implant soft tissue barrier. Clinically, it demonstrates vast clinical differences to periodontitis that suggests distinct inflammatory mechanisms. Implant-derived Titanium particles (i-TiPs) frequently found around diseased implants appear to alter the microenvironment and confer resistance to antibiotic treatments. Studies in orthopedic implants have demonstrated a strong inflammatory response to i-TiPs, involving a variety of cell types, in aseptic conditions. Nonetheless, the genetic programs of cells surveilling and supporting the peri-implant soft tissue barrier in response to the combined challenges of biomaterial degradation products and oral bacteria are poorly defined. Thus, we studied gene expression specific to oral peri-implant inflammatory disease. We found that certain cellular pathways were highly upregulated in diseased tissues. Upregulated pathways provided insight into important physiological pathways that might play a role in peri-implant pathology. These findings could potentially contribute to the production of more targeted and effective therapeutics for the disease.
2021-06-17 | GSE178351 | GEO
Project description:Comparative metatranscriptomic analysis in peri-implantitis and periodontitis
| PRJDB3765 | ENA
Project description:Objectives: The aim of this study was to identify the long noncoding RNAs (lncRNAs) and mRNAs that influence the different manifestations of peri-implantitis and periodontitis (I vs. P). Materials and methods: Gingival tissues from 6 peri-implantitis patients, 6 periodontitis patients, and 6 healthy individuals were analysed using lncRNAs and mRNAs gene expression microarrays. A lncRNAs subgroup analysis, a lncRNAs cluster graph, gene ontology (GO), and a pathway analysis of mRNAs were performed to analyse the data extracted from microarrays. To verify the results of the microarray studies, quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess some differentially expressed lncRNAs and mRNAs. Results: In the gene expression microarray studies, 1,079 differentially expressed lncRNAs and 1,003 differentially expressed mRNAs were identified when comparing I vs. P. The lncRNAs subgroup analysis showed that there were 9 significantly up-regulated antisense lncRNAs and 18 significantly down-regulated antisense lncRNAs when comparing I vs. P. GO analysis on mRNAs revealed that the cyclooxygenase pathway is the most prominent signal among the up-regulated transcripts (3 genes) and that hemidesmosome assembly represents the most significant biological process among the down-regulated transcripts (4 genes) when comparing I vs. P. The expression levels of antisense lncRNA GACAT2 and mRNA MTCL1, antisense lncRNA MSC-AS1 with its sense mRNA MSC and TRPA1 were verified by RT-qPCR. Conclusions: Results indicated that peri-implantitis and periodontitis exhibit significantly different lncRNAs and mRNAs expression profiles. Additionally, specific lncRNAs may take part in the pathogenesis mechanisms of peri-implantitis and periodontitis through influencing their nearby mRNAs.
2020-10-24 | GSE106090 | GEO
Project description:Core function of microbiota in peri-implantitis and periodontitis
| PRJDB4192 | ENA
Project description:Tolerance to dietary antigens is critical to avoid deleterious type 2 immune responses resulting in food allergy (FA) and anaphylaxis. However, the mechanisms resulting in both the maintenance and failure of tolerance to food antigens is poorly understood. Here we demonstrate that the goblet cell-derived resistin-like molecule beta (RELMb) is a critical regulator of oral tolerance. We find that RELMb is abundant in serum in both food allergic patients and mouse models of FA. Deletion of RELMβ protects mice from FA, development of food antigen specific IgE and anaphylaxis. RELMb disrupts food tolerance through modulation of the gut microbiome by suppressing gut Lactobacilli. Tolerance is maintained via local production of indole derivatives driving FA protective RORgt+ regulatory T (Treg) cells via activation of the aryl hydrocarbon receptor (AhR). RELMb antagonism in the peri-weaning period restored oral tolerance and protected genetically prone offspring from developing FA later in life. Together, our data identify RELMb as mediating both a novel gut immune-epithelial circuit regulating tolerance to food antigens, a new mode of innate control of antigen specific adaptive immunity via microbiome editing and targetable candidates in this circuit for prevention and treatment of FA.
2022-12-27 | GSE221462 | GEO
Project description:Comparison of bacterial flora of peri-implantitis and periodontitis using DNA
| PRJDB6966 | ENA