16S rDNA amplicon next generation micorbiome analysis of smokers with periodontitis
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB35812 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3822950_1.fastq.gz | Fastqsanger.gz | |||
| ERR3822950_2.fastq.gz | Fastqsanger.gz | |||
| ERR3822960_1.fastq.gz | Fastqsanger.gz | |||
| ERR3822960_2.fastq.gz | Fastqsanger.gz | |||
| ERR3822970_1.fastq.gz | Fastqsanger.gz |
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Project description:This prospective study aimed to investigate salivary proteome changes in periodontitis patients in response to treatment. Ten systemically healthy, non-smokers with stage III, grade C periodontitis (32-43yrs, F:M:5:5) underwent non-surgical periodontal treatment. Saliva (n=30) was collected pre- (T0), and one (T1) and six (T6) month post-treatment. Whole-mouth plaque (PI) and gingival index (GI), probing depth (PD), bleeding on probing (BOP) and clinical attachment loss (CAL) were measured. The saliva proteome was investigated by label-free quantitative proteomics. Normalized protein intensities were measured and protein changes modeled over time (linear model) with significant protein regulation considered at false discovery rate (FDR)<0.05. Treatment significantly reduced PI, GI, BOP, percentages of sites with PD≥5mm and PD≥5mm+BOP (T1vsT0 and T6vsT0), PD and CAL (T6vsT0). Overall, 1713 proteins (5927 peptides) were identified. Following analysis, considering proteins quantified by ≥2 peptides, resulted in 878 distinct proteins. At T1, 80 (T1vsT0:60↑:20↓), and at T6, 118 human proteins (T6vsT0:67↑:51↓) were regulated. Top-regulated disease categories were shared between T1vsT0 and T6vsT0, with highest activity patterns for ‘cellular movement’. The post-treatment proteome (T6vsT1) remained stable. Periodontal treatment reduced clinical disease parameters and these changes were reflected in the salivary proteome.
2024-06-10 | PXD043901 | Pride
Project description:Periodontitis (PD) as a chronic inflammatory disease instigated by periodontal pathogenic bacteria and mediated by the host immune response, resulting in the destruction of supporting periodontal tissue and tooth loss in adults. Constructing an injectable delivery system that allows for sustained drug release within periodontal pockets to continuously eliminate pathogenic bacteria, reduce periodontal inflammation, and promote periodontal tissue regeneration is an effective strategy for periodontitis treatment. Here, we explore the therapeutic potential and underlying mechanisms of curcumin-loaded Pickering emulsion (PE-CUR) in periodontitis treatment. The Pickering emulsion formulation offers an effective delivery system, enhancing curcumin's bioavailability and therapeutic efficacy. In vitro studies, we demonstrate that the PE-CUR exhibit excellent biocompatibility and anti-inflammatory property by elimination of reactive oxygen species (ROS). In addition, PE-CUR significantly eliminate key periodontal pathogens, including Porphyromonas gingivalis (P. gingivalis) and Staphylococcus aureus (S. aureus). In a rat model of periodontitis, PE-CUR significantly attenuates periodontal tissue inflammation and alveolar bone loss, indicating a protective effect against periodontal tissue destruction. Mechanistically, PE-CUR promotes the expression of anti-inflammatory factors and inhibits the release of pro-inflammatory factors by regulating macrophage polarization from M1 to M2 and modulating the MAPK and PI3K-AKT signaling pathway. Furthermore, PE-CUR decreases the formation of osteoclasts as well as stimulates the activation and differentiation of osteoblasts successively, thereby ameliorating the periodontal inflammation and promoting the alveolar bone regeneration. Overall, our findings elucidate the therapeutic mechanisms of PE-CUR in periodontitis, suggesting its potential as a promising treatment strategy warranting further clinical investigation.
2024-08-16 | GSE274645 | GEO
Project description:Over the last years, proteomic techniques have been demonstrated to be valuable tools for analysing the periodontal proteome in gingival crevicular fluid (GCF) samples contributing to identifying extensive and comprehensive protein profiles associated with periodontitis. However, the periodontal proteome has not yet been studied using sequential window acquisition of all theoretical mass spectra (SWATH-MS). Consequently, the objective of the present longitudinal research was to investigate the periodontal proteome in GCF in three clinical conditions (periodontal health, untreated periodontitis, and treated periodontitis), applying SWATH-MS to 1) analyse the periodontal proteome structure in the three clinical groups, 2) compare the differential protein expression between the three clinical groups, and 3) evaluate the diagnostic accuracy of the proteins quantified to identify new biomarkers with a high capacity to discriminate the three clinical conditions. A total of 84 subjects, 44 periodontally healthy and 40 with generalised untreated periodontitis in stages III-IV, were included, and GCF samples were collected. The diagnosis of periodontal status was conducted by two experienced dentists using clinical and radiographic criteria. The definition of periodontal status was established following the Classification of Periodontal Diseases and Conditions published in 2018. In the untreated periodontitis group, 38 underwent conventional non-surgical treatment and were evaluated clinically after two months (treated periodontitis group). In the revaluation, 25 individuals showed significant clinical improvement in probing pocket depth (PPD) at the selected sites, and GCF samples were collected from them.
2024-10-17 | PXD043474 | Pride
Project description:Gene expressions relate to the pathogenesis of periodontitis and have a crucial role in local tissue destruction and susceptibility to the disease. The aims of the present study were to explore comprehensive gene expressions/transcriptomes in periodontitis-affected gingival tissues, and to identify specific biological processes. The purpose of the present study was 1) to compare comprehensive gene expression/transcriptomes of periodontitis-affected gingival tissues with those of healthy tissues by using microarray and data mining technologies, and 2) to analyze significantly differentially expressed genes which belong to pathological pathways in periodontitis by qRT-PCR. Two distinct gingival samples including healthy and periodontal-affected gingiva were taken from 3 patients with severe chronic periodontitis. Total RNAs from 6 gingival tissue samples were used for microarray and data-mining analyses. Comparisons, gene ontology, and pathway frequency analyses were performed and identified significant biological pathways in periodontitis. Quantitative reverse transcription real-time polymerase chain reaction (qRT-PCR) analyse using 14 chronic periodontitis patients including 3 patients listed above and 14 healthy individuals showed 9 differentially expressed genes in leukocyte migration and cell communication pathways.
2010-08-13 | E-GEOD-23586 | biostudies-arrayexpress
Project description:The present study aimed to compare the miRNA expression profile in individuals with chronic (CP) and aggressive (AP) periodontitis. Eighteen non-smokers individuals (CP = 9 and AP = 9) without any history of systemic diseases or previous periodontal therapy were selected at the Clinics of Periodontology from the Federal University of Minas Gerais. Gingival tissue samples were collected during the initial periodontal therapy. miRNAs were isolated and expression patterns of 754 miRNAs were assessed with a quantitative miRNA PCR array. miRNAs expression profiles were compared between CP and AP groups. No differences were observed in the miRNAs expression profiles between CP and AP groups (p>0.05). According to miRNA microarray analyses, the most expressed miRNAs in both groups were hsa-miR-1274b, hsa-let-7b, hsa-miR-24, hsa-miR-19b, hsa-miR-720, hsa-miR-126, hsa-miR-17 and hsa-miR-21. Findings suggested that there were no differences in miRNAs expression profiles between chronic and aggressive forms of periodontitis. The overexperssion of especific miRNAs could provide insights on the pathogenesis of both forms of the disease.
2018-06-26 | GSE116209 | GEO
Project description:Objective Ulcerative colitis (UC) is a risk factor of periodontitis. This study aimed to investigate whether hematopoietic stem and progenitor cells (HSPCs) and their myeloid progeny exacerbate periodontal inflammation in UC. Design Ligature-induced periodontitis (LIP) was established in dextran sulfate sodium (DSS)-induced colitis (DIC) C57BL/6 mice. The bone resorption, intestinal and periodontal inflammation were evaluated by micro-CT and histological analyses. Inflammatory cytokines and lipopolysaccharide (LPS) in serum and gut microbiota were assessed by multiplexed flow cytometric assay, ELISA and 16S rRNA sequencing, respectively. Flow cytometry was performed to analyze HSPCs differentiation, and to sort hematopoietic stem cells for transcriptomic analysis. Berberine treatment of DIC was employed to investigate whether dampening of DIC would alleviate periodontitis. Results DIC mice exhibited disrupted intestinal barrier with dysbiotic gut microbiota, corroborating the elevated serum level of LPS and IL-1. Compared to DIC-free/LIP mice, DIC/LIP mice showed aggravated alveolar bone resorption, with enrichment of neutrophils extracellular traps (NETs) in periodontal tissues. DIC promoted myelopoiesis of HSPCs by up-regulating myeloid differentiation pathway. Intragastric administration of berberine dampened DIC and rescued the myeloid skewing of HSPCs, consequently alleviating periodontal destruction. Intriguingly, LIP induction after DIC remission still exhibited aggravated periodontal destruction and myeloid skewing of HSPCs, indicating a UC-trained immunity against periodontal infection. Conclusion Increased gut permeability and microbial dysbiosis in UC elevate the serum level of LPS and IL-1, inducing myeloid skewing of HSPCs with an immune memory. Generation of inflammatory potential myeloid cells causes NETs accumulation and aggravates periodontal destruction in the UC-related periodontitis.
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2024-03-06 | GSE254766 | GEO
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.
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Project description:Inflammatory periodontal disease (periodontitis) is widespread in dogs. This study aimed to evaluate site-specific changes in the canine gingival crevicular fluid (GCF) proteome during the longitudinal progression from very mild gingivitis to mild periodontitis. Periodontitis diagnosis in dogs requires anaesthesia, our ultimate aim was to develop a periodontitis diagnostic that could be applied to samples taken from conscious dogs. The objective of this work was to identify potential biomarkers of periodontal disease progression in the GCF of dogs.
2016-03-21 | PXD003337 | Pride