Dataset Information

Probing the Salivary Proteome for Prognostic Biomarkers in Response to Non-Surgical Management of Periodontitis

ABSTRACT: 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.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Saliva

DISEASE(S): Periodontitis

SUBMITTER: Angelika Silbereisen

LAB HEAD: Nagihan Bostanci

PROVIDER: PXD043901 | Pride | 2024-06-10

REPOSITORIES: Pride

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Probing the salivary proteome for prognostic biomarkers in response to non-surgical periodontal therapy.

Silbereisen Angelika A Bao Kai K Wolski Witold W Nanni Paolo P Kunz Laura L Afacan Beral B Emingil Gülnur G Bostanci Nagihan N

Journal of clinical periodontology 20240425

<h4>Aim</h4>This prospective study investigated the salivary proteome before and after periodontal therapy.<h4>Materials and methods</h4>Ten systemically healthy, non-smoking, stage III, grade C periodontitis patients underwent non-surgical periodontal treatment. Full-mouth periodontal parameters were measured, and saliva (n = 30) collected pre- (T0), and one (T1) and six (T6) months post-treatment. The proteome was investigated by label-free quantitative proteomics. Protein expression changes w ...[more]

PMID: 38660744

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Project description:Phase 1: The whole saliva samples were obtained from 66 systemically healthy subjects consisting of patients with chronic periodontitis (CP), generalized aggressive periodontitis (G-AgP), gingivitis and individuals with periodontal health. The use of humans for study satisfied the requirements of the Ege University Institutional Review Board (Ethics number 16-12.1/16) and and was conducted in accordance with the guidelines of the World Medical Association Declaration of Helsinki. It is confirmed that this cross-sectional study conforms to STROBE guidelines for observational studies. Complete medical and dental histories were taken from all participants. Systemic exclusion criteria were the presence of cardiovascular and respiratory diseases, diabetes mellitus, HIV infection, systemic inflammatory conditions or non-plaque-induced oral inflammatory conditions, immunosuppressive chemotherapy, and current pregnancy or lactation. Smoking status was also recorded. None of the patients had taken medication such as antibiotics or anti-inflammatory drugs that could affect their periodontal status for at least 6 months before the study. Patients eligible for the study returned to the clinic for clinical measurement screening one-week after being pre-screened. Before being enrolled in the study, participants provided written and informed consent to use their saliva samples and individual data for scientific purposes. The clinical periodontal indices including probing depth (PPD), clinical attachment level (CAL), plaque index (PI) and bleeding on probing (BOP) were recorded by a manual periodontal probe by a trained and calibrated examiner (V.O.O). The extent and severity of alveolar bone support were evaluated radiographically in each patient. The participants were classified into four groups based on their periodontal conditions according to the criteria proposed by the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions (REF). Generalized Aggressive Periodontitis (G-AgP): The G-AgP group included 17 patients with ≥16 teeth. The patients had a non- contributory medical history and demonstrated with an early age of clinical manifestations with a generalized pattern of rapid attachment loss and bone destruction. These individuals had minimum of CAL ≥ 5 mm and PD ≥ 6 mm on eight or more teeth; at least three of these were other than central incisors or first molars. Radiographic bone loss was above ≥ 30 % of root length affecting ≥3 permanent teeth other than first molars and incisors. Generalized Chronic Periodontitis (CP): The CP group included 17 patients with severe generalized chronic periodontitis. These individuals had a minimum four non-adjacent teeth with sites with CAL ≥ 5 mm and PPD ≥ 6 mm, and ≥50 % alveolar bone loss in at least two quadrants which was commensurate with the amount of plaque accumulation. Phase 2: We aimed to develop SRM-based workflow for detecting and quantitating the relative abundance of the candidate proteins in an independent saliva cohort . 82 subjects (48 females and 34 males; age range 24-59 years) were recruited for the study at the Department of Periodontology, School of Dentistry, Adnan Menderes University, Aydın, Turkey. Ethical clearance was obtained from the Ethics Committee of the School of Medicine, Ege University with the protocol number ((Ethics number 70198063-050.06.04). Each participant gave written and verbal informed consent after the purpose and procedures of the study were explained. A dental and medical history was compiled for all subjects as detailed in phase 1 and participants were clustered into four groups according to the criteria proposed by the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions as detailed at Phase 1

Project description:This study was conducted to determine the impact of extreme temperatures, aiming at controlling microorganisms by cooking, on the physiology and the transcriptome of Escherichia coli. ABSTRACT: Because the genome of Escherichia coli K12 is well understood, this organism was used as a model to investigate physiological and molecular changes during cell adaptation and survival to cooking temperatures used in the food industry. Bacteria grown at 37Â°C to stationary phase in Brain Heart Infusion (BHI) broth, were heated at 58Â°C or 60Â°C to reach a process lethality value (F) of 2 and 3, or until an internal core temperature of 71Â°C was reached (control cooking temperature). Both growth recovery and cell membrane integrity were evaluated immediately after heating and a global transcription analysis was performed by using gene expression microarrays. Only cells heated at 58Â°C F = 2 were still able to grow on liquid or solid BHI after heat treatment. However, their transcriptome did not differ significantly compared to those of bacteria heated at 58Â°C F = 3 (P-FDR > 0.01) where no growth recovery was observed post treatment. Genome-wide transcriptomic data obtained at 71Â°C were distinct from the other treatments. Quantification of heat-shock genes expression by real-time PCR revealed that dnaK and groEL mRNA levels were significantly lower at 71Â°C than at 58Â°C and 60Â°C (P < 0.0001). Furthermore, despite of similar cell inactivation but growth on BHI media after heating, 132 and 8 genes were differentially expressed at 71Â°C when compared to 58Â°C and 60Â°C at F = 3 respectively (P-FDR < 0.01). Among them, genes like aroA, citE, glyS, oppB and asd, whose expression was up-regulated at 71Â°C, may be considered as good biomarkers to determine more accurately the efficiency of heat treatments. Bacteria were submitted to four different heat-treatments. Biological replicates: 5 Controls grown to an optimal temperature of 37Â°C (and used to prepare a common reference for each array hybridization), 5 Treatment 1 (58Â°C F = 2), 4 Treatment 2 (58Â°C F = 3), 4 Treatment 3 (60Â°C F = 3), 5 Treatment 4 (core temperature of 71Â°C). Treatment replicates were randomly hybridized on 3 microarray slides Agilent 8x15K (total of 24 array areas). Equal amounts of the labeled control cDNA pool and labeled cDNA from one of the heated groups were mixed and hybridized on each array.

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.

Project description:The present research aimed to investigate peripheral blood gene expression profiling as a minimally invasive surrogate approach to study silica-induced pulmonary toxicity. Rats were exposed to crystalline silica by inhalation (15 mg/m3, 6 hours/day, 5 days). Pulmonary damage and blood gene expression profiles were determined at various latency periods (0 - 16 weeks). Silica exposure resulted in pulmonary toxicity and this was evidenced by histological changes in the lungs and elevation of LDH activity, and total protein and albumin contents in the bronchoalveolar lavage fluid (BALF) of the rats. Microarray analysis of global gene expression profiles in the blood of the rats identified genes that were differentially expressed in response to silica exposure and toxicity. The number of significantly differentially expressed genes in the blood of silica exposed rats correlated with the severity of silica-induced pulmonary toxicity. Genes involved in biological functions such as inflammatory response, cancer, pulmonary damage, oxidative stress, energy metabolism, fibrosis, etc, were found differentially expressed in the blood of the silica exposed rats compared with the controls. Induction of pulmonary inflammation in the silica exposed rats, as suggested by differential expression of inflammatory response genes in the blood, was supported by significant increases in the number of macrophages and infiltrating neutrophils as well as the activity of pro-inflammatory chemokines M-bM-^@M-^S MCP1 and MIP2, observed in the BALF of the silica exposed rats. A silica-responsive blood gene expression signature developed using the gene expression data predicted with significant accuracy the exposure of rats to lower concentrations (1 and 2 mg/m3) of silica. Taken together our findings suggest the potential application of peripheral blood gene expression profiling as a minimally invasive and efficient surrogate approach to detect and study silica-induced pulmonary toxicity. 96 samples were analyzed in this experiment. The RNA from rat blood samples was isolated for gene expression studies. Rats (48) were exposed to crystalline silica by inhalation (15 mg/m3, 6 hours/day, 5 days) and air (24). Blood gene expression profiling was performed using rat blood samples, 8 each for silica exposed and 4 each for air exposed controls at various post-exposure time periods (0, 1, 2, 4, 8, and 16 weeks). A silica-responsive blood gene expression signature was developed using the gene expression data obtained from the 0 week post-exposure group and the control rats. The signature was tested for predicting silica exposure and resulting toxicity in the rats exposed to lower concentrations (1 and 2 mg/m3) of silica (8 rats per group) and air (8 rats).

Dataset Information

Probing the Salivary Proteome for Prognostic Biomarkers in Response to Non-Surgical Management of Periodontitis

Publications

Probing the salivary proteome for prognostic biomarkers in response to non-surgical periodontal therapy.

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