Inhibitory effects of Fusobacterium nucleatum on osteogenic differentiation of osteoblasts and its molecular mechanism
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ABSTRACT:
PROVIDER: PRJNA550409 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9590000_1.fastq.gz | Fastqsanger.gz | |||
| SRR9590000_2.fastq.gz | Fastqsanger.gz | |||
| SRR9590010_1.fastq.gz | Fastqsanger.gz | |||
| SRR9590010_2.fastq.gz | Fastqsanger.gz | |||
| SRR9590020_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: F.nucleatum is one of the important pathogens of periodontitis, and the main symptom of periodontitis is alveolar bone loss. The study of F.nucleatum in alveolar bone loss caused by periodontitis is still very insufficient. In this study, the biological behavior of osteoblasts stimulated by F.nucleatum was studied to elucidate the mechanism of bone loss in periodontitis. Methods:A primary rat calvarial osteoblast culture model was established and invaded repeatedly with F.nucleatum (ATCC 25586). Transcriptome analysis at multiple time points(days 1, 3, 7, 14, 21 and 28) was applied to identify gene expression changes in osteoblasts stimulated by F.nucleatum. Cell-counting and EDU-labeling assay were used to analyze the effects of F.nucleatum on the cell proliferation. Flow cytometry and enzyme linked immunosorbent assay (ELISA) was used to analysis the cell apoptosis, cell cycle and secreted inflammatory cytokines changes. ALP activity testing, Alizarin red mineralized nodules staining and calcium content assays, qPCR and western blot were carried on to evaluate the osteogenic differentiation and mineralization of osteoblasts. Results: Cytology experiments and RNA-seq analysis showed that F.nucleatum could inhibit cell proliferation, promote cell apoptosis, block cell cycle of osteoblasts and promote inflammatory cytokines production in a dose- and time-dependent manner. Besides, F. nucleatum could significantly inhibited osteoblasts differentiation and mineralization via a series inhibition of the differentiation regulatory genes and proteins. Whole-transcriptome analysis identified a total of 235 transcripts that were differentially expressed in all six time-points, most of which were inflammatory-related genes. The genes, Ccl2, Ccl20, Csf1, Cx3cl1, Cxcl1, Cxcl3, Il6, Birc3, Map3k8, Nos2, Nfkb2, Tnfrsf1b and Vcam1, played core roles in a PPI network and interacted closely with other ones in the infection. In addition, 133 osteogenesis-related DEGs were time-serially dynamically changed in a short time-series expression miner (STEM) analysis, which were enriched in multiple cancer-related pathways. The core dynamic DEGs (Mnda, Cyp1b1, Comp, Phex, Mmp3, Tnfrsf1b, Fbln5 and Nfkb2) had been reported to be closely related to the development and metastasis in tumor and cancer progress. This study is the first to evaluate the long-term interaction of F. nucleatum on osteoblasts, which might increase the risk of cell carcinogenesis of normal osteoblasts, and provides new insight into the pathogenesis of bacterial-induced bone destruction.
2020-10-22 | GSE133223 | GEO
Project description:Localization of Fusobacterium nucleatum in the placenta may be associated with pregnancy complications including preeclampsia (PE), but its specific pathobiology is unknown. Our aim was to analyze the effect of Fusobacterium nucleatum on HUVEC cells to further elucidate placental dysfunction in the context of Fusobacterium nucleatum infestation.
2024-06-08 | GSE269085 | GEO
Project description:Fusobacterium nucleatum is a Gram-negative oncobacterium that is associated with colorectal cancer. The molecular mechanisms utilized by F. nucleatum to promote colorectal tumor development have largely focused on adhesin-mediated binding to the tumor tissue and on the pro-inflammatory capacity of F. nucleatum. However, the exact manner in which F. nucleatum promotes inflammation in the tumor microenvironment and subsequent tumor promotion remains underexplored. Here, we show that both live F. nucleatum and sterile F. nucleatum-conditioned medium promote CXCL8 release from the intestinal adenocarcinoma HT-29 cell line. We determined that the pro-inflammatory response was ALPK1-dependent in both HEK293 and HT-29 cells and that the released F. nucleatum molecule had characteristics that match those of the pro-inflammatory ALPK1 ligand ADP-heptose or related heptose phosphates. In addition, not only F. nucleatum but also other Fusobacterium species such as F. varium, F. necrophorum and F. gonidiaformans promoted an ALPK1-dependent pro-inflammatory environment, indicating that ADP-heptose or related heptose phosphates secretion is a conserved feature of the Fusobacterium genus. By performing transcriptional analysis of ADP-heptose stimulated HT-29 cells, we found several inflammatory and cancer-related pathways to be differentially regulated, including DNA mismatch repair genes and the immune inhibitory receptor PD-L1. Finally, we show that stimulation of HT-29 cells with F. nucleatum resulted in an ALPK1-dependent upregulation of PD-L1. These results aid in our understanding of the mechanisms by which F. nucleatum can affect tumor development and therapy and pave the way for future therapeutic approaches.
2024-05-13 | GSE267317 | GEO
Project description:Neutrophils are known to be stimulated by different periodontal bacteria to produce reactive oxygen species and cytokines. It is inportant to investigate the gene changes made by bacteria of importance, of which, for periodontal disease, fusobaterium nucleatum is one. we used microarrays to investigate gene experssion changes in peripheral blood neutrophils werwhich e stimulated with or with out Fusobacterium Nucleatum (10953). Neutrophils from periodonatlly healthy individuals (n=4) were isolated and stimulated for 3hrs with or without fusobaterium nucleatum (10953). RNA was then extracted from these and pooled before hybridization on Affymetrix microarrays
2010-07-20 | E-GEOD-20151 | biostudies-arrayexpress
Project description:Fusobacterium nucleatum is a Gram-negative oral bacterial species associated with periodontal disease progression. As periodontal disease progresses, it is known F. nucleatum coaggregated with blood is frequently detected in the gingival crevice. However, it is largely unknown whether these interactions between F. nucleatum and blood induce a particular genetic response. We tested the cultures of F. nucleatum ATCC 25586 with or without blood in a semi-defined growth medium by microarray analysis and found 14 genes that were affected after only about 4hr. of adhered blood. Then, we selected 7 genes that changed significantly and tested these genes via real-time RT-PCR to confirm the validity of the microarray results. As a result, one amino sugar-binding protein on the membrane of F. nucleatum was especially expressed high via both microarray and real-time RT-PCR. Based upon these data, it appears that the protein on the F. nucleatum membrane binds and transfers the amino sugar only under blood conditions. This study aims to determine the effect of blood on the gene expression profiling of F. nucreatum. The study contains 2 separate experiments that both measure the cultures without or with blood. The samples with blood contain 9% and 33% blood.
2012-09-01 | E-GEOD-36410 | biostudies-arrayexpress
Project description:Fusobacterium nucleatum-treated LoVo cells reported an increased promoting CRC metastasis effect compared with PBS control. To understand the underlying mechanisms of Fusobacterium nucleatum-induced metastasis ability of CRC cells, we performed RNA-sequencing in LoVo cells s with or without Fusobacterium nucleatum treatment with three independent biological replicates.
2021-10-19 | GSE173549 | GEO
Project description:To investigate the effect of the Zn ionophore, PBT2, on the transcriptomic response of Fusobacterium nucleatum ATCC 25586, RNA was extracted from bacterial samples which had been treated as follows: Untreated (0.006% DMSO v/v), DMSO-Zn treated (0.006% DMSO v/v + 200 uM ZnSO4), or PBT2-Zn treated (0.125 ug/mL PBT2 + 200 uM ZnSO4) (DMSO was the vehicle control). RNA samples were collected at 0h, 0.5h, and 1h post challenge in biological triplicate and sequenced using Illumina HiSeq platform. We mapped sequences to the reference genome F. nucleatum subsp. nucleatum ATCC 25586 and performed DEseq2 analysis to determine differentially expressed genes across time and treatment.
2021-07-15 | E-MTAB-8681 | biostudies-arrayexpress
Project description:To investigate the role of Fusobacterium nucleatum-mediated m6A modification, we performed m6A-sequencing to map the m6A modification in control or Fusobacterium nucleatum-treated HCT116 cells.
2022-02-07 | GSE150308 | GEO
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