Mouse gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA895549 | ENA |
REPOSITORIES: ENA
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Project description:Periodontitis increases the risk of non-alcoholic fatty liver disease (NAFLD). However, the precise mechanisms are unclear. Here, gut dysbiosis induced by orally administered Porphyromonas gingivalis, a representative periodontopathic bacterium, was implicated in the deterioration of NAFLD pathology. C57BL/6 mice were administered with the vehicle, P. gingivalis or Prevotella intermedia, with weaker periodontal pathogenicity, followed by feeding on a choline-deficient, high fat diet (CDAHFD60). CDAHFD60 feeding induced hepatic steatosis, and combined bacterial administration further aggravated NAFLD pathology with increased fibrosis. Liver gene expression analyses revealed that genes involved in the NAFLD pathology were perturbed with distinctive expression profiles induced by different bacteria. These differences may be due to quantitative and qualitative differences in the influx of gut bacterial products because the serum endotoxin level, gut microbiota composition, and serum metabolite profile caused by ingested P. intermedia and P. gingivalis were different. These findings provide insights into mechanisms linking periodontitis and NAFLD.
2021-11-03 | GSE136937 | GEO
Project description:Periodontitis patients exhibit significant upregulation of the cholinergic signaling pathway in gingival epithelial cells, accompanied by elevated acetylcholine (ACh) levels in saliva. However, the role of ACh in the pathogenesis of periodontitis remains unclear. P. gingivalis, a keystone pathogen in periodontitis, triggers host inflammatory responses and compromises the epithelial barrier function. As the first line of defense against pathogens, the reparative capacity of the oral epithelium critically influences the progression of periodontitis. This study investigates whether ACh modulates P. gingivalis-induced inflammatory responses and epithelial repair in human oral keratinocytes (HOKs), aiming to elucidate the mechanistic role of cholinergic signaling in periodontitis.
2025-05-21 | GSE297378 | GEO
Project description:The outer membrane vesicles (OMVs) produced by Porphyromonas gingivalis (P. gingivalis) contain a variety of bioactive molecules that may be involved in the progression of periodontitis. However, the participation of P. gingivalis OMVs in the development of periodontitis has not been elucidated. Here we isolated P. gingivalis OMVs and confirmed their participation in periodontitis both in vivo and in vitro. Microcomputed Tomography (micro-CT) and histological analysis showed that under the stimulation of P. gingivalis OMVs, the alveolar bone of rats was significantly resorbed in vivo. We found that P. gingivalis OMVs were taken up by hPDLCs (human Periodontal Ligament Cells, hPDLCs) in vitro, then subsequently resulting in apoptosis and inflammatory cytokines releasing which was accomplished by the microRNA-size small RNAs (msRNAs) sRNA45033 in the P. gingivalis OMVs. Through bioinformatics analysis and screening of target genes, Chromobox 5 (CBX5) was identified as the downstream target of screened-out small RNA s45033. Using dual-luciferase reporter assay, overexpression, and knockdown methods, s45033 was confirmed to target CBX5 to regulate hPDLCs apoptosis. In addition, Cleavage Under Targets and Tagmentation (Cut&Tag) analysis confirmed the mechanism that CBX5 regulates apoptosis through the methylation of p53 DNA. Collectively, these findings indicate that the role of P. gingivalis OMVs is immunologically relevant and related to bacterial virulence in the development of periodontitis.
2022-11-30 | GSE218606 | GEO
Project description:Porphyromonas gingivalis (P. gingivalis) is a key pathogen in periodontitis. Our previous study indicated that periodontitis induced by P. gingivalis increases the percentage of CD19+ B cells, Th17, Treg, gMDSCs and mMDSCs but decreases the ratio of B10 cells in CIA mice. It’s unclear which virulence factors of P. gingivalis are involved in these processes. Here, our study first indicated that such effects are mainly resulted from the undenatured proteins other than the DNA, RNA or LPS of P. gingivalis. As gingipains are enzymes and virulence factors which play vital role in the progression in periodontitis through affecting innate and adaptive immune system, we then compared the influence of the wild-type strain of P. gingivalis (ATCC33277) with its isogenic gingipain-null mutant (△K△RAB) on B cells. The results showed that B cells infected with △K△RAB exhibited increased levels of IL-6 and others cytokines (IL-1β，IL-23) involve in Th17 differentiation compared to wild-type strain, also the frequency of IL-10 producing regulatory B cells (B10). Furthermore, the peritonitis induced by △K△RAB enhanced the proportion of B10 and Th17 compared with treated with ATCC33277. Cumulatively, this study preliminarily revealed deletion of gingipains affected the antigen presentation of B cell that promoted B cells express the cytokines which promoted T cells toward Th17 and the secretion immunosuppressive cytokines of B cells that enhanced the frequency of B10 which implicated gingipains are vital in altering B cell function to participated immune response.
2023-05-29 | GSE195704 | GEO
Project description:Porphyromonas gingivalis is a gram-negative bacterium that causes destructive chronic periodontitis. In addition, this bacterium is also involved in the development of cardiovascular disease. The aim of this study was to investigate the effects of P. gingivalis infection on gene and protein expression in human aortic smooth muscle cells (AoSMCs) and its relation to cellular function.
2013-11-17 | E-MTAB-1922 | biostudies-arrayexpress
Project description:Porphyromonas gingivalis secretes cysteine proteases named gingipains which can cleave an array of proteins and importantly contribute to the development of periodontitis. In this study we focused on gingipain-exerted proteolysis at the cell surface of human gingival epithelial cells (telomerase immortalized gingival keratinocytes [TIGK]). We examined whether gingipains have sheddase activity or if their main activity is degradation of membrane proteins into small fragments. Using mass spectrometry, we investigated the whole sheddome/degradome of TIGK cell surface proteins by P. gingivalis strains differing in gingipain expression. We observed extensive degradation of TIGK surface proteins, suggesting that gingipains could in fact be the major cause of damage to the gingival epithelium. Most of the identified gingipain substrates were molecules involved in adhesion, suggesting that gingipains may cause tissue damage through cleavage of cell contacts, resulting in cell detachment and rounding, and consequently leading to anoikis. These results reveal a molecular underpinning to P. gingivalis-induced tissue destruction and enhance our knowledge of the role of P. gingivalis’ proteases in the pathobiology of periodontitis.
2020-04-28 | PXD015679 | Pride
Project description:Six- to eight-week-old wild-type male C57BL/6 mice were randomly grouped into four groups (n = 6): the periodontitis (PD), periodontitis with Lr treatment (LR), fat diet with periodontitis (HPD) and fat diet with periodontitis and Lr treatment (HLR)
| PRJNA1196631 | ENA
Project description:Six- to eight-week-old wild-type male C57BL/6 mice were randomly grouped into four groups (n = 6): the periodontitis (PD), periodontitis with IPA treatment (IPA), fat diet with periodontitis (HPD) and fat diet with periodontitis and IPA treatment (HI
| PRJNA1196627 | ENA
Project description:Porphyromonas gingivalis impairs glucose uptake in muscle by altering gut microbiota
| PRJDB9383 | ENA
Project description:Effect of HGF on gut microbiota in mice with periodontitis
| PRJNA1019142 | ENA