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The effect of periodontitis - induced trained immunity on the transcriptomic profile of mouse LSK cells [RNA-seq]

ABSTRACT: Hematopoietic stem and progenitor cells (HSPCs) in the bone marrow can sense peripheral inflammation and adapt through expansion and skewing toward the myeloid lineage. In this study, we performed RNA sequencing in LSK (Lin—Sca-1+cKit+ ) cells to determine the impact of ligature-induced periodontitis on the transcriptomic profile of HSPCs in mice bone marrow.

ORGANISM(S): Mus musculus

PROVIDER: GSE180002 | GEO | 2022/04/27

REPOSITORIES: GEO

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The effect of periodontitis - induced trained immunity on the epigenomic profile of mouse bone marrow LSK and GMP cells

Project description:Peripheral inflammation affects hematopoietic stem and progenitor cells (HSPCs) in the bone marrow and induce myeloid lineage skewing of the progenitor cells. In this study, we performed single cell ATAC-sequencing in LSK (Lin—Sca-1+cKit+ ) and GMP (Lin—c-Kit+Sca1—CD16/32+CD34+) cells to determine the impact of ligature-induced periodontitis (LIP) on the epigenomic profile of these BM cells.

2022-04-27 | GSE180025 | GEO

The single-cell transcriptome profiling of mouse bone marrow LSK cells after resolution of periodontitis

Project description:Periodontitis induces myeloid lineage skewing of the bone marrow progenitor cells. In this study, we performed single cell RNA-sequencing in LSK (Lin—Sca-1+cKit+ ) cells to determine whether the periodontitis-induced myeloid lineage bias persists after the resolution of periodontal inflammation.

2022-04-27 | GSE196808 | GEO

Ulcerative colitis aggravates periodontitis via myeloid skewing of hematopoietic progenitor cell differentiation

Project description:Objective Ulcerative colitis (UC) is a risk factor of periodontitis. This study aimed to investigate whether hematopoietic stem and progenitor cells (HSPCs) and their myeloid progeny exacerbate periodontal inflammation in UC. Design Ligature-induced periodontitis (LIP) was established in dextran sulfate sodium (DSS)-induced colitis (DIC) C57BL/6 mice. The bone resorption, intestinal and periodontal inflammation were evaluated by micro-CT and histological analyses. Inflammatory cytokines and lipopolysaccharide (LPS) in serum and gut microbiota were assessed by multiplexed flow cytometric assay, ELISA and 16S rRNA sequencing, respectively. Flow cytometry was performed to analyze HSPCs differentiation, and to sort hematopoietic stem cells for transcriptomic analysis. Berberine treatment of DIC was employed to investigate whether dampening of DIC would alleviate periodontitis. Results DIC mice exhibited disrupted intestinal barrier with dysbiotic gut microbiota, corroborating the elevated serum level of LPS and IL-1. Compared to DIC-free/LIP mice, DIC/LIP mice showed aggravated alveolar bone resorption, with enrichment of neutrophils extracellular traps (NETs) in periodontal tissues. DIC promoted myelopoiesis of HSPCs by up-regulating myeloid differentiation pathway. Intragastric administration of berberine dampened DIC and rescued the myeloid skewing of HSPCs, consequently alleviating periodontal destruction. Intriguingly, LIP induction after DIC remission still exhibited aggravated periodontal destruction and myeloid skewing of HSPCs, indicating a UC-trained immunity against periodontal infection. Conclusion Increased gut permeability and microbial dysbiosis in UC elevate the serum level of LPS and IL-1, inducing myeloid skewing of HSPCs with an immune memory. Generation of inflammatory potential myeloid cells causes NETs accumulation and aggravates periodontal destruction in the UC-related periodontitis.

2023-12-10 | GSE249582 | GEO

Investigation of the role of Il33 in the chronicity of the periodontitis

Project description:To investigate the function of different tissues in the pathogenesis, we established a modified mouse ligature-induced periodontitis model, supporting the separation of the maxillae into gingiva, peri-root, and bone tissue. After setting the right molars as the non-ligature control side and the left molars as the ligature side, we performed gene expression profiling and gene enrichment analysis using data obtained from RNA-seq of sixteen individuals after 11 days of induction (32 samples in total). Four individuals were WT mice, and another four were Il33-deficient mice. Sample of peri-root tissues and bone tissues from these mice were compared separately to explore the role of Il33 in the chronicity of periodontitis, especially its function in periodontal ligament and bone tissue.

2024-02-23 | GSE244931 | GEO

High-resolution analysis of the pathogenesis of periodontitis

Project description:To investigate the function of different tissues in the pathogenesis, we established a novel mouse ligature-induced periodontitis model, supporting the separation of the maxillae into gingiva, peri-root, and bone tissue. After setting the right molars as the non-ligature control side and the left molars as the ligature side, we performed gene expression profiling and gene enrichment analysis using data obtained from RNA-seq of four individuals after 5-days-induction (24 samples in total).

2024-02-23 | GSE221720 | GEO

Single Cell RNA sequencing of mouse periodontitis gingiva

Project description:Purpose: The goal of this study was to characterize the gingival oral barrier immunity of mouse periodontitis gingiva. Method: A silk thread (ligature) was tied wround the mouse maxillary molar. Mouse palatal gingiva was harvested at 1 days after the ligature placement. Gingival cells were harvested and subjected to 10X Genomix scRNA-seq. Cell Ranger processed data were analysed.

2023-11-09 | GSE228635 | GEO

Single Cell RNA sequencing of mouse early periodontitis gingiva

Project description:Purpose: The goal of this study was to characterize the gingival oral barrier immunity of mouse early periodontitis gingiva. Method: A silk thread (ligature) was tied wround the mouse maxillary molar. Mouse palatal gingiva was harvested at 1 days after the ligature placement. Gingival cells were harvested and subjected to 10X Genomix scRNA-seq. Cell Ranger processed data were analysed.

2022-04-21 | GSE201108 | GEO

Type VI Collagen Deficiency Causes Enhanced Periodontal Tissue Destruction in Induced Periodontitis

Project description:Single cell analysis of PDL cells in ligature-induced periodontitis: The periodontal ligament (PDL) is a fibrillar connective tissue that lies between the alveolar bone and the tooth and is composed of highly specialized extracellular matrix (ECM) molecules and a heterogeneous population of cells that are responsible for collagen formation, immune response, bone formation, and chewing force sensation. Type VI collagen (COL6), a widely distributed ECM molecule, plays a critical role in the structural integrity and mechanical properties of various tissues including muscle, tendon, bone, cartilage, and skin. However, its role in the PDL remains largely unknown. Our study shows that deficiency of COL6 impairs PDL fibrogenesis and exacerbates tissue destruction in ligature-induced periodontitis (LIP). We found that COL6 deficient mice exhibited increased bone loss and degraded PDL in LIP and that fibroblasts expressing high levels of Col6α2 are pivotal in ECM organization and cell-ECM interactions. Moreover, COL6 deficiency in the PDL led to an increased number of fibroblasts geared towards the inflammatory response. We also observed that cultured COL6 deficient fibroblasts from the PDL exhibited decreased expression of genes related to collagen fiber metabolism and ECM organization, and migration and proliferation. Our findings suggest that COL6 plays a crucial role in the PDL, influencing fibroblast function in fibrogenesis and affecting the immune response in periodontitis. These insights could advance our understanding of the molecular mechanisms underlying PDL maturation and periodontal disease.

2024-06-24 | GSE255695 | GEO

Gingival transcriptomics phases of periodontitis lesions in nonhuman primate model

Project description:We used a nonhuman primate (NHP) model of ligature-induced periodontitis to identify gingival transcriptome changes associated with aging during the phases of periodontitis lesions (initiation, progression, and resolution). Four age groups of nonhuman primate were studied: Young (<3 years of age); Adolescent (3 to 7 years), Adult (12 to 15 years), and Aged (17-23 years)

2021-07-22 | GSE180588 | GEO

Comparison of mRNA expression levels in peri-implantitis and periodontitis within the same host environment

Project description:Purpose: The aim of this study was to explore whether differences exist and to what an extent of the immune-mediated inflammatory reactions between periodontitis and peri-implantitis at the transcriptional level in the same susceptible host. Methods: Ligature-induced experimental peri-implantitis and periodontitis in the same mice were established. Gingival tissues of healthy, periodontitis and peri-implantitis sites from the same oral cavity were collected and used for RNA-sequencing. Differentially expressed genes (DEGs) were screened between periodontitis/peri-implantitis sites and healthy sites. The enrichment analysis of DEGs were analyzed. Comprehensive immune landscape was annotated by seq-ImmuCC. Results: The results showed that 137 and 353 up-regulated DEGs as well as and 670 and 174 down-regulated DEGs were specifically expressed periodontitis/peri-implantitis group compared to the healthy control group, respectively. The pathways of complement and coagulation cascade and osteoclast differentiation were dominating in the peri-implantitis sites. Moreover, peri-implantitis sites exhibited elevated macrophage proportions and relatively enriched macrophage activation and bone loss compared with periodontitis. Conclusions: Results indicated that peri-implantitis and periodontitis exhibited significantly distinct transcriptional signatures. Additionally, the study suggests that the interplay between macrophages and bone resorption are comparatively more active in peri-implantitis compared with periodontitis. These biological processes may be factors contributing to the pathogenesis of peri-implantitis being distinct from that of periodontitis.

2022-06-06 | GSE186882 | GEO

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