Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Type I interferon protects against bone loss in periodontitis by mitigating an interleukin (IL)-17-neutrophil axis [scRNA-seq]

ABSTRACT: Type I interferon protects against bone loss in periodontitis by mitigating an interleukin (IL)-17-neutrophil axis [scRNA-seq]

PROVIDER: PRJNA1242370 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32870009_1.fastq.gz	Fastqsanger.gz
	SRR32870009_2.fastq.gz	Fastqsanger.gz
	SRR32870010_1.fastq.gz	Fastqsanger.gz
	SRR32870010_2.fastq.gz	Fastqsanger.gz
	SRR32870011_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Type I interferon protects against bone loss in periodontitis by mitigating an interleukin (IL)-17-neutrophil axis [RNA-Seq]

Project description:Type I interferon protects against bone loss in periodontitis by mitigating an interleukin (IL)-17-neutrophil axis [RNA-Seq]

| PRJNA1243377 | ENA

Type I interferon protects against bone loss in periodontitis by mitigating an interleukin (IL)-17-neutrophil axis [RNA-Seq]

Project description:We assessed the transcriptomic profile at the late stage on day 10 at the end of the ligature-induced periodontitis model through RNA-seq.

2025-03-28 | GSE293227 | GEO

Type I interferon protects against bone loss in periodontitis by mitigating an interleukin (IL)-17-neutrophil axis [scRNA-seq]

Project description:We determined the early inflammatory infiltrates on day 3 after ligature placement, a stage prior to noticeable bone loss, by performing single -cell RNA sequencing (scRNA -seq)

2025-03-28 | GSE293027 | GEO

Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

Project description:Neutrophil recruitment and activation are hallmarks of the prevalent inflammatory disease, periodontitis. However, the mechanisms by which neutrophils contribute to in inflammatory bone destruction remain unclear. Herein, we document that neutrophil extracellular traps (NETs) have a direct role in mediating inflammatory pathology. In an established animal model of periodontitis, we demonstrate that genetic or pharmacologic inhibition of NETs formation, or removal of NETs by DNase-Ⅰ, alleviates inflammatory bone loss in vivo. Investigating the mechanisms by which NETs drive periodontal inflammation, we find that extracellular histones have a direct role in disease progression. Consistent with findings in animal models, histones bearing classic NET-associated post-translational modifications are correlated with disease severity and are significantly elevated in local lesions and systemic circulation of patients with periodontitis. Our work reveals NETs-associated components as pathogenic mediators, potential biomarkers, and therapeutic targets for periodontitis.

2023-05-23 | GSE228021 | GEO

Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

Project description:Neutrophil extracellular traps trigger inflammatory bone destruction in periodontitis

| PRJNA947673 | ENA

The neutrophil–osteogenic cell axis promotes bone destruction in periodontitis

Project description:The neutrophil–osteogenic cell axis promotes bone destruction in periodontitis

| PRJNA1071651 | ENA

Transcription profiling of human peripheral blood neutrophils reveals periodontitis is associated with a type-1 interferon signature

Project description:Peripheral blood neutrophils from periodontitis patients exhibit a hyper-reactive and hyper-active phenotype (collectively termed hyper-responsivity) in terms of production of reactive oxygen species (ROS) however the molecular basis for this observation is yet to be determined. Our objectives were to identify genes differentially expressed in hyper-responsive peripheral blood neutrophils from chronic periodontitis patients relative to periodontally healthy controls and use this data to identify potential contributory pathways to the hyper-responsive neutrophil phenotype. Experiment Overall Design: Neutrophils taken from 4 chronic periodontitis patients and age/sex matched healthy controls. RNA extracted and subsequently hybridised in dulpicate on to U133A arrays.

2008-10-25 | E-GEOD-12484 | biostudies-arrayexpress

The neutrophil–osteogenic cell axis promotes bone destruction in periodontitis

Project description:We performed single-cell RNA-sequencing analysis on mouse periodontal lesions to analyze the detailed mechanism underlying immune–bone cell interactions in periodontitis.

2024-03-06 | GSE254766 | GEO

Periodontitis is associated with a type-1 interferon signature in peripheral blood neutrophils

2008-08-20 | GSE12484 | GEO

Global changes in human neutrophil transcriptome profile during Filifactor alocis challenge

Project description:Periodontitis is a multifactorial chronic inflammatory infectious disease with a high prevalence in the adult population in the USA. Until recently, research into periodontitis focused primarily on putative pathogens such as Porphyromonas gingivalis. However, a reappraisal of microbial etiology has marked a turning point in the field due to the development of culture-independent techniques that allow the identification of bacterial species directly from nucleic acids. Filifactor alocis, a Gram positive anaerobic oral bacterium, has emerged as an important periodontal pathogen. Neutrophils are recruited in high numbers to the gingival tissue, where they are linked with protection against periodontal disease. However, periodontal pathogens evolved different strategies to resist neutrophil microbicidal mechanisms while propagating inflammation, which affords a source of nutrients. The goal of this study was to determine the global changes in human neutrophil gene expression induced by F. alocis challenge. RNA-sequencing analysis shows that F. alocis-challenge alters human neutrophil transcriptome including expression of genes associated with regulation of Toll-Like Receptor signaling pathway, MAPK signaling pathway, apoptosis, cytokines and chemokines, among other neutrophil effector functions.

2020-04-06 | GSE137351 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data