Human oral metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1270987 | ENA |
REPOSITORIES: ENA
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Project description:The oral cavity is considered an extra-gastric reservoir for Helicobacter pylori (H. pylori) and oral H. pylori can contribute to the gastric eradication inability and recurrence. However, the oral environment is not ideal for H. pylori survival, and the factors promoting oral colonization and survival of H. pylori have not been elucidated. In this study, we explored the effects of extracellular polysaccharides (EPS), the fundamental building blocks of dental Streptococcus mutans (S. mutans) biofilm, on H. pylori colonization and drug resistance in the oral cavity, as well as stomach. In the co-culture system of H. pylori Sydney strain (SS1) and three S. mutans biofilms with different EPS contents (UA159 wild-type, UA159ΔgtfB, UA159ΔgtfBC), it was found that the adhesive force between SS1 and biofilms increased correspondingly with the increase in EPS content. Moreover, with the increase in EPS content of biofilms, the number of colonized SS1 increased. Proteome analysis revealed that SS1 co-cultured with UA159 biofilm exhibited 149 differentially expressed proteins compared to that co-cultured with UA159ΔgtfB biofilm, with significant enrichment in β-lactamase activity pathway. SS1 co-cultured with UA159 biofilm exhibited 154 differentially expressed proteins compared to that co-cultured with UA159ΔgtfBC biofilm, with significant enrichment in β-lactamase activity, aminoglycoside nucleotidyltransferase activity and antioxidant activity pathways. Both in vivo and in vitro, EPS synthesized by glucosyltransferases (Gtfs) surrounding SS1 was verified to protect SS1 against β-lactam and aminoglycoside antibiotics. These findings demonstrated that S. mutans biofilms mediate oral adhesion, colonization, and antibiotic resistance of H. pylori through a Gtfs-driven EPS biosynthesis mechanism.
| PXD066577 |
Project description:The interaction of clinically relevant microorganisms is the focus of various studies, e.g. the interaction between the pathogenic yeast, Candida albicans, and the bacterium, Pseudomonas aeruginosa and these interactions can alter the outcome of infection, growth dynamics of each species and antimicrobial resistance of pathogens. During infection, both C. albicans and P. aeruginosa can elicit the release arachidonic acid (AA) from host cells membranes through the action of phospholipases. This polyunsaturated fatty acid can be transformed into immune-modulating compounds, termed eicosanoids, by both host-derived and microbial-derived enzymatic reactions. In its free form, AA can affect the growth of both C. albicans and P. aeruginosa, inhibiting the morphogenesis of C. albicans as well as reducing resistance towards antifungal agents. However, the mechanism of this is unknown. Previous studies on the effect of polyunsaturated fatty acids have indicated a possible alteration in plasma membrane organisation and permeability. Our group aimed to address how AA affects C. albicans in both single species biofilms, as well as in polymicrobial biofilms with P. aeruginosa. RNAseq was performed on single and polymicrobial biofilms in the presence and absence of a sub-inhibitory (100 µM) concentration of AA. Differential expression was determined between C. albicans single species biofilms in the presence and absence of AA. Secondly, the influence of co-incubation of C. albicans with P. aeruginosa in the absence of AA was evaluated to identify novel facets of interaction not previously identified, and to establish a baseline to determine the effect of AA on C. albicans in polymicrobial biofilms. Lastly, the effect of AA on C. albicans in polymicrobial biofilms was determined through comparison with polymicrobial biofilms in the absence of AA. This study provides a comprehensive analysis of the effect of AA and both co-incubation of C. albicans with P. aeruginosa focused on the transcriptome.
2021-01-31 | GSE136726 | GEO
Project description:Carbapenem-resistant Acinetobacter baumannii (CRAb) is an urgent public health threat, according to the CDC. This pathogen has few treatment options and causes severe nosocomial infections with >50% fatality rate. Although previous studies have examined the proteome of CRAb, there have been no focused analyses of dynamic changes to β-lactamase expression that may occur due to drug exposure. Here, we present our initial proteomic study of variation in β-lactamase expression that occurs in CRAb with different β-lactam antibiotics. Briefly, drug resistance to Ab (ATCC 19606) was induced by the administration of various classes of β-lactam antibiotics, and the cell-free supernatant was isolated, concentrated, separated by SDS-PAGE, digested with trypsin, and identified by label-free LC-MS-based quantitative proteomics. Thirteen proteins were identified and evaluated using a 1789 sequence database of Ab β-lactamases from UniProt, the majority of which were Class C β-lactamases (≥80%). Importantly, different antibiotics, even those of the same class (e.g. penicillin and amoxicillin), induced non-equivalent responses comprising various isoforms of Class C and D serine-β-lactamases, resulting in unique resistomes. These results open the door to a new approach of analyzing and studying the problem of multi-drug resistance in bacteria that rely strongly on β-lactamase expression.
2023-07-20 | PXD042336 | Pride
Project description:In vitro oral biofilms exposed to chlorhexidine
| PRJNA554992 | ENA
Project description:OSCC is associated with substantial mortality and morbidity. To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of OSCC, oral dysplasia, and normal oral tissue from patients without oral cancer or preneoplastic oral lesions (controls). Results provided models of gene expression to distinguish OSCC from controls.
2011-07-22 | GSE30784 | GEO
Project description:When Proteus mirabilis, Enterococcus faecalis, and Escherichia coli are co-cultured in human urine, they form biofilms with increased biomass. This increase in biomass is due to a rise in the total protein content of the biofilm rather than other components, such as carbohydrates or nucleic acids. The study focused on identifying proteins that are enriched in polymicrobial biofilms (co-cultures) compared to monomicrobial biofilms. Proteins that increase in relative abundance during co-culture may serve as targets for preventing the formation of recalcitrant polymicrobial biofilms.
2026-08-24 | PXD074670 | Pride
Project description:<p>Bacterial metabolism in oral biofilms is comprised of complex networks of nutritional chains and biochemical regulations. These processes involve both intraspecies and interspecies networks as well as interactions with components from host saliva, gingival crevicular fluid, and dietary intake. In a previous paper, a large salivary glycoprotein, mucin MUC5B, was suggested to promote a dental health-related phenotype in the oral type strain of <em>Streptococcus gordonii</em> DL1, by regulating bacterial adhesion and protein expression. In this study, nuclear magnetic resonance-based metabolomics was used to examine the effects on the metabolic output of monospecies compared to dual species early biofilms of two clinical strains of oral commensal bacteria, <em>S. gordonii</em> and <em>Actinomyces naeslundii</em>, in the presence of MUC5B. The presence of <em>S. gordonii</em> increased colonization of <em>A. naeslundii</em> on salivary MUC5B, and both commensals were able to utilize MUC5B as a sole nutrient source during early biofilm formation. The metabolomes suggested that the bacteria were able to release mucin carbohydrates from oligosaccharide side chains as well as amino acids from the protein core. Synergistic effects were also seen in the dual species biofilm metabolome compared to the monospecies, indicating that <em>A. naeslundii</em> and <em>S. gordonii</em> cooperated in the degradation of salivary MUC5B. A better understanding of bacterial interactions and salivary-mediated regulation of early dental biofilm activity is meaningful for understanding oral biofilm physiology and may contribute to the development of future prevention strategies for biofilm-induced oral disease.</p>
2023-10-30 | MTBLS8370 | MetaboLights
Project description:Genome-wide expression array measurements for 9 head and neck squamous cell carcinomas (HNSCC) stratified by worst pattern of invasion (WPOI) Jayakar et al. (2016). Apolipoprotein E promotes invasion in oral squamous cell carcinoma. Li et al. (2013). Validation of the risk model: high-risk classification and tumor pattern of invasion predict outcome for patients with low-stage oral cavity squamous cell carcinoma. Comparison of transcription profiles between OSCC tumors with a more invasive (WPOI 5) versus a less invasive (WPOI 3) pattern of invasion using two independent Illumina platforms.
2016-04-01 | E-GEOD-79795 | biostudies-arrayexpress
Project description:OSCC is associated with substantial mortality and morbidity. To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of OSCC, oral dysplasia, and normal oral tissue from patients without oral cancer or preneoplastic oral lesions (controls). Results provided models of gene expression to distinguish OSCC from controls. RNA from 167 OSCC, 17 dysplasia and 45 normal oral tissues were extracted and hybridized to Affymetrix U133 2.0 Plus GeneChip arrays. The differentially expressed genes were identified using GenePlus software and the validation was done using RT-PCR, using independent internal and external datasets.
2011-07-21 | E-GEOD-30784 | biostudies-arrayexpress
Project description:Heterogeneity in oral cancer associated fibroblasts (CAFs)in tumor microenvironment modulate plasticity of malignant epithelial cells to drive tumorigenesis, ultimately leading to poorer clinical outcome. Myofibroblastically differentiated CAFs induce stochastic plasticity in oral cancer cells. We co-cultured non-myofibroblasts and myofibroblasts with oral cancer cell lines to understand distinct CAF driven cancer cell transcriptional reprogramming.
2025-04-11 | GSE294386 | GEO