Ontology highlight
ABSTRACT:
PROVIDER: PRJNA528513 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8771420.fastq.gz | Fastqsanger.gz | |||
| SRR8771421.fastq.gz | Fastqsanger.gz | |||
| SRR8771422.fastq.gz | Fastqsanger.gz | |||
| SRR8771413.fastq.gz | Fastqsanger.gz | |||
| SRR8771423.fastq.gz | Fastqsanger.gz |
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Project description:Apical periodontitis (AP) is a painful inflammatory disease resulting from tooth infection that affects millions worldwide with a marked impact on quality of life and is accompanied by bone loss surrounding the affected tooth. There is growing evidence that the nociceptive fibers densely innervating teeth regulate the disease progression, in addition to their sensorial function. We hypothesized that nociceptors regulate the transcriptomic profile of the periapical osteolytic lesion in a mouse model of AP. Male control (Nav1.8 cre+/-) and nociceptor-ablated (Nav1.8cre+/- DTAlox+/-) mice were generated and underwent pulp exposure procedures on all 4 first molars and at 8 weeks of age. At either 0, 7, or 14 days after pulp exposure, periapical tissues were dissected from mice (n=3-4/strain/time point). Total RNA was extracted from the pooled periapical lesions from each animal and submitted for total RNA sequencing and bioinformatic analysis. We found that pulp exposure triggers the differential expression of hundreds of genes within the periapical lesion over the course of infection with marked differences between in both control and mice with nociception ablation. Importantly, at 14 days post pulp-exposure, 422 genes were differentially expressed between nociceptor-ablated and control mice with greater enrichment of biological processes related to inflammation, specifically immune cell chemotaxis and migration, compared to control mice. Among these inflammatory markers, TNFα, IL-1α, and IL-1β, that are known to play a crucial role in AP were significantly upregulated in nociceptor-ablated mice. In conclusion, nociceptor-ablation regulates the transcriptomic profile of periapical lesions in a mouse model of AP, shifting the gene expression profile to a greater enrichment of inflammatory genes, suggesting nociceptors play a role in the kinetics of the immune response. This newly uncovered neuro-immune axis and its mechanisms in AP can potentially be an important therapeutic target for the treatment of this prevalent disease.
2023-12-31 | GSE205195 | GEO
Project description:The goal of this study was to analyze global gene expression in specific populations of nociceptor sensory neurons, the neurons that detect damaging/noxious stimuli. The dorsal root ganglia (DRG), trigeminal ganglia, and nodose ganglia are anatomically distinct peripheral sensory ganglia that contain nociceptors which innervate skin, gut, lungs, and other distinct organ tissues. We used flow cytometry to purify nociceptors from these ganglia and profiled their global gene expression signatures to compare gene expression between these different anatomically distinct nociceptors. Nav1.8-Cre were bred with Rosa26-TdTomato to generate Nav1.8-Cre/R26-TdTomato reporter progeny, where all peripheral nociceptor neurons are genetically marked with red fluroescence due to specific expression of the TTX- resistant sodium channel Nav1.8. Lumbar region dorsal root ganglia (DRG), trigeminal ganglia, and nodose ganglia were dissected from mice (3 mice were pooled/sample). Highly red fluorescent neurons were Facs purified, RNA extracted, and processed for microarray analysis.
2013-08-28 | E-GEOD-46546 | biostudies-arrayexpress
Project description:Nociceptor neurons play a crucial role in maintaining the body’s homeostasis by detecting and responding to potential dangers in the environment. However, this function can be detrimental during allergic reactions, since vagal nociceptors can contribute to immune cell infiltration, bronchial hypersensitivity, and mucus imbalance, in addition to causing pain and coughing. Despite this, the specific mechanisms by which nociceptors acquire pro-inflammatory characteristics during allergic reactions are not yet fully understood. In this study, we aimed to investigate the molecular profile of airway nociceptor neurons during allergic airway inflammation and identify the signals driving such reprogramming. Using retrograde tracing and lineage reporting, we identified a unique class of inflammatory vagal nociceptor neurons that exclusively innervate the airways. In the ovalbumin mouse model of airway inflammation, these neurons undergo significant reprogramming characterized by the upregulation of the NPY receptor Npy1r. A screening of cytokines and neurotrophins revealed that IL-1β, IL-13 and BDNF drive part of this reprogramming. IL-13 triggered Npy1r overexpression in nociceptors via the JAK/STAT6 pathway. In parallel, sympathetic neurons and macrophages release NPY in the bronchoalveolar fluid of asthmatic mice, which limits the excitability of nociceptor neurons. Single-cell RNA sequencing of lung immune cells has revealed that a cell-specific knockout of Npy1r in nociceptor neurons in asthmatic mice leads to an increase in airway inflammation mediated by T cells. Opposite findings were observed in asthmatic mice in which nociceptor neurons were chemically ablated. In summary, allergic airway inflammation reprograms airway nociceptor neurons to acquire a pro-inflammatory phenotype, while a compensatory mechanism involving NPY1R limits nociceptor neurons’ activity.
2024-11-04 | GSE278510 | GEO
Project description:Apical periodontitis (AP) is a painful disease that develops quickly following dental infections and is primarily characterized by robust inflammation surrounding the tissues of the affected tooth, resulting in disruption of bone homeostasis and periradicular bone loss. Moreover, there are distinct clinical presentations, symptoms, and responses to AP treatment between males and females, creating a desperate need to further understand the sex-specific mechanisms of AP. With the growing evidence that nociceptors modulate AP development, we utilized RNA sequencing in nociceptor-ablated (Nav1.8 cre+/-, Diphtheria Toxin Alox+/-) transgenic mice to study nociceptor regulation of the periapical lesion transcriptome using a rodent model of AP in female mice over 14 days. Overall, we found that female mice exhibit unique patterns of differentially expressed genes throughout AP infection compared to male mice, and that the expression of these genes is regulated by nociceptors. Additionally, nociceptor-ablation results in a more significant enrichment of biological processes related to immune responses earlier compared to cre-control (Nav1.8 cre+/-) females as well as greater expression of genes involved in inflammatory processes and osteolytic activity. Therefore, while nociceptor-ablation augments inflammatory and bone resorption responses in both males and females in a mouse model of AP, transcriptomic analyses demonstrate the mechanisms through which nociceptors modulate AP are distinct between sexes. These studies will provide the foundation needed to study further mechanisms of sex differences in AP, an area with a desperate need for investigation to treat current AP patients. Understanding these mechanisms can ultimately inform treatment options to alleviate suffering for millions of patients suffering from AP.
2024-02-01 | GSE254607 | GEO
Project description:The first GSSM of V. vinifera was reconstructed (MODEL2408120001). Tissue-specific models for stem, leaf, and berry of the Cabernet Sauvignon cultivar were generated from the original model, through the integration of RNA-Seq data. These models have been merged into diel multi-tissue models to study the interactions between tissues at light and dark phases.
2024-09-02 | MODEL2408160001 | BioModels
Project description:Small intestine is highly innervated by nociceptor neurons. Single cell RNA sequencing (scRNA-seq) of ileal epithelial cells was performed to analyze the role of nociceptor neurons in regulating small intestinal epithelial cells.
2022-10-01 | GSE208594 | GEO
Project description:The colon is densely innervated by nociceptor neurons. Single cell RNA sequencing (scRNA-seq) of colon epithelial cells was performed to analyze the role of nociceptor neurons and Ramp1 signaling in regulating colonic epithelial cells.
2022-10-01 | GSE208762 | GEO
Project description:The goal of this study was to analyze global gene expression in specific populations of nociceptor sensory neurons, the neurons that detect damaging/noxious stimuli. The dorsal root ganglia (DRG), trigeminal ganglia, and nodose ganglia are anatomically distinct peripheral sensory ganglia that contain nociceptors which innervate skin, gut, lungs, and other distinct organ tissues. We used flow cytometry to purify nociceptors from these ganglia and profiled their global gene expression signatures to compare gene expression between these different anatomically distinct nociceptors.
2013-08-28 | GSE46546 | GEO
Project description:Opioid-dependent immune-mediated analgesic effects have been broadly reported upon inflammation. In preclinical mouse models of intestinal inflammatory diseases, the local release of enkephalins (endogenous opioids) by colitogenic T lymphocytes alleviate inflammationinduced pain by down-modulating gut-innervating nociceptor activation in periphery. In this study, we wondered whether this immune cell-derived enkephalin-mediated regulation of the nociceptor activity also operates under steady state conditions. Here, we show that chimeric mice engrafted with enkephalin-deficient bone marrow cells exhibit not only visceral hypersensitivity but also an increase in both epithelial paracellular and transcellular permeability, an alteration of the microbial topography resulting in increased bacteriaepithelium interactions and a higher frequency of IgA-producing plasma cells in Peyer’s patches. All these alterations of the intestinal homeostasis are associated with an anxiety-like behavior despite the absence of an overt inflammation as observed in patients with irritable bowel syndrome. Thus, our results show that immune cell-derived enkephalins play a pivotal role in maintaining gut homeostasis and normal behavior in mice. Because a defect in the mucosal opioid system remarkably mimics some major clinical symptoms of the irritable bowel syndrome, its identification might help to stratify subgroups of patients.
2023-11-22 | GSE244917 | GEO