Human oral metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1088630 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28392424_1.fastq.gz | Fastqsanger.gz | |||
| SRR28392424_2.fastq.gz | Fastqsanger.gz | |||
| SRR28392425_1.fastq.gz | Fastqsanger.gz | |||
| SRR28392425_2.fastq.gz | Fastqsanger.gz | |||
| SRR28392426_1.fastq.gz | Fastqsanger.gz |
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Project description:At mucosal surfaces, epithelial cells provide a structural barrier and an immune defense system. However, dysregulated epithelial responses can contribute to disease states. Here, we demonstrate that epithelial intrinsic production of IL-23 triggers an inflammatory loop in the prevalent oral disease, periodontitis. Epithelial IL-23 expression localized to areas proximal to the disease-associated microbiome, is evident both in experimental models and in patients with common and genetic forms of disease. Mechanistically, flagellated microbial species of the periodontitis microbiome, trigger epithelial IL-23 induction in a TLR5-dependent manner. Intriguingly, unlike other Th17-driven diseases, here non-hematopoietic cell-derived IL-23 serves as an initiator of pathogenic inflammation. Beyond periodontitis, analysis of publicly available datasets reveals expression of epithelial IL-23 in settings of infection, malignancy, and autoimmunity, suggesting a broader role for epithelial-intrinsic IL-23 in human disease. Collectively, this work highlights an unappreciated role for the barrier epithelium in the induction of IL-23-mediated inflammation.
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Project description:Oral polymorphonuclear neutrophils (oPMNs) are essential for the maintenance of oral health. Functionally active oPMNs have been described in oral health, gingivitis and periodontitis. Interestingly, recent evidence showed that oPMNs from chronic periodontitis patients have a similar functional and reactivity pattern compared to oPMNs from healthy subjects. However, it remains unknown whether oPMNs respond to the initiation and resolution of gingival inflammation. Therefore, this study aimed to evaluate the oPMNs’ transcriptional responses during the initiation and resolution of an experimentally induced gingivitis. Oral rinses were obtained from 8 subjects at 4 different time points during the experiment for the isolation of oPMNs; day 0 (baseline), day 9 (during gingivitis challenge), day 14 (end of the challenge) and day 21 (resolution). Transcriptome of oPMNs was determined by RNAsequencing. Differentially expressed genes (DEGs) was selected at P<0.01 level, and evaluated for pathway regulation at different time points using Ingenuity Pathway Analysis suite. During the gingivitis challenge, dental plaque levels and gingival bleeding levels were significantly increased at day 14 compared to baseline. Transcriptome analysis indicate four major clusters of DEGs, which consisted of a group of 256 initial response DEGs (day 9 only), 221 late response DEGs (day 14 only), 53 persistent response DEGs (consistent at day 9 and day 14), and a group of 524 DEGs showing response only after the gingivitis challenge (day 21 only). Pathway analysis of the initial response DEGs showed their involvement in many immune regulatory pathways (interleukin signaling, reactive oxygen species processes and granulocyte adhesion and diapedesis). Late responding DEGs mainly showed activation of signaling pathways and phagosome formation as part of the phagocytosis process, whereas DEGs at day 21 were involved in epithelial adherence signaling and other miscellaneous related signaling pathways. This study showed that oPMNs have specific expression profiles during the development and resolution of experimental gingivitis. Even though, the specific observed pathways were not identical within each time point, the altered pathways indicate PMN responses in general and suggests an immunomodulatory role for the oPMNs. The oPMNs may therefore play a co-controlling part in the initiation and resolution of gingival inflammation.
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Project description:Periodontitis patients often develop bacteremia, but there has been little evidence showing that oral bacteria translocate into other organs. We found that bacterial colony formation occurs in a culture of liver and spleen cells of periodontitis-induced mice, and the bacterial species detected in the liver and spleen were found in the oral cavity as well, but not in fecal samples, indicating systemic dissemination of oral bacteria during the breakdown of the oral barrier.
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Project description:The effect of oral microbiota on the intestinal microbiota has garnered growing attention as a mechanism linking periodontal diseases to systemic diseases. However, the salivary microbiota is diverse and comprises numerous bacteria with a largely similar composition in healthy individuals and periodontitis patients. Thus, the systemic effects of small differences in the oral microbiota are unclear. In this study, we explored how health-associated and periodontitis-associated salivary microbiota differently colonized the intestine and their subsequent systemic effects by analyzing the hepatic gene expression and serum metabolomic profiles. The salivary microbiota was collected from a healthy individual and a periodontitis patient and gavaged into C57BL/6NJcl[GF] mice. Samples were collected five weeks after administration. Gut microbial communities were analyzed by 16S ribosomal RNA gene sequencing. Hepatic gene expression profiles were analyzed using a DNA microarray and quantitative polymerase chain reaction. Serum metabolites were analyzed by capillary electrophoresis time-of-flight mass spectrometry. The gut microbial composition at the genus level was significantly different between periodontitis-associated microbiota-administered (PAO) and health-associated oral microbiota-administered (HAO) mice. The hepatic gene expression profile demonstrated a distinct pattern between the two groups, with higher expression of Neat1, Mt1, Mt2, and Spindlin1, which are involved in lipid and glucose metabolism. Disease-associated metabolites such as 2-hydroxyisobutyric acid and hydroxybenzoic acid were elevated in PAO mice. These metabolites were significantly correlated with Bifidobacterium, Atomobium, Campylobacter, and Haemophilus, which are characteristic taxa in PAO mice. Conversely, health-associated oral microbiota were associated with higher levels of beneficial serum metabolites in HAO mice. The multi-omics approach used in this study revealed that periodontitis-associated oral microbiota is associated with the induction of disease phenotype when they colonized the gut of germ-free mice.
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Project description:Animal model implicates microbiota-triggered oral mucosal Th17 cells as drivers of local immunopathology and therapeutic targets in periodontitis.
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Project description:Although periodontitis is a widespread disease, its molecular mechanisms in human oral cells are not fully understood. Therefore, we established cell lines from the human oral cavity, including gingival keratinocytes (GK), osteoblastic lineage cells from the alveolar bone (OLAB), PDL fibroblasts (PDLF) and cementum cells (CC). Using label-free quantitative mass spectrometry, we investigated changes of the proteome of healthy human oral cells after co-cultivation with Aggregatibacter actinomycetemcomitans and Eikenella corrodens for 24 h, for the first time. Our findings show specific protein profiles for each of the human oral cell lines. This will help to understand pathologic mechanisms in periodontitis and related diseases, such as rheumatoid arthritis, diabetes mellitus or atherosclerotic vascular diseases.
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Project description:Our present findings show for the first time that the virulence factor PPAD protects the oral pathogen P. gingivalis against neutrophil insults at three distinct levels, namely phagocytosis, NETosis and CAMP activity. This identifies PPAD as a major agent in the evasion of human innate immunity, a view that is supported by studies from Potempa and co-workers showing PPAD-dependent citrullination of complement29. Why is this important? Every day, millions of people lose teeth due to periodontitis. This has a serious impact on their quality of life, not only for aesthetic reasons but much more so because tooth loss causes difficulties in eating and interferes with interpersonal communication. Yet, only few people realize that there is a major bacteriological component in periodontitis where our immune defences are breached with potentially serious implications, especially systemic and chronic diseases ranging from bacteraemia to rheumatoid arthritis.
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