Ontology highlight
ABSTRACT:
PROVIDER: PRJNA921889 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23018400.fastq.gz | Fastqsanger.gz | |||
| SRR23018401.fastq.gz | Fastqsanger.gz | |||
| SRR23018402.fastq.gz | Fastqsanger.gz | |||
| SRR23018403.fastq.gz | Fastqsanger.gz | |||
| SRR23018404.fastq.gz | Fastqsanger.gz |
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Project description:SARS-CoV-2 infects the nasal epithelium (NE) and can cause olfactory dysfunction. Because the virus cannot infect olfactory sensory neurons (OSNs) which detect odorants, the underlying mechanisms remain unknown. Here, using human embryonic stem cells, we were the first to develop human NE organoids comprising both olfactory neuroepithelia (OE) and nasal respiratory epithelia (NRE). SARS-CoV-2 initially replicated in the NRE and then spread to the OE where angiotensin converting enzyme 2 was expressed after virus replication in NRE. Importantly, a significant proportion of neural precursor cells (NPCs) and basal stem cells in the OE, both of which constantly differentiate into OSNs, were infected. Viral infection upregulated cell death-associated genes in the NPCs and basal stem cells, suggesting that SARS-CoV-2 infection disrupts the repair and renewal of OSNs. Taken together, our human nasal organoid model would be useful for the investigation of a potential mechanism underlying olfactory dysfunction in COVID-19 patients.
2025-10-06 | GSE309325 | GEO
Project description:<p>Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by both motor and non-motor symptoms, including olfactory dysfunction, which often precedes motor symptoms by several years. However, the underlying mechanisms linking olfactory dysfunction in PD to biological changes remain unclear. Recent studies suggest a potential connection between PD's olfactory dysfunction and alterations in the nasal microbiome and metabolome, but comprehensive investigations are still lacking.This study aims to explore the interplay between nasal microbiota, metabolites, and olfactory function in PD, identify potential biomarkers for early diagnosis, and investigate therapeutic targets for olfactory dysfunction in PD.</p><p> </p><p>Methods: From October 1, 2023, to September 30, 2024, 66 potential participants were enrolled, including PD patients with varying degrees of olfactory dysfunction and healthy controls. Nasal samples were collected for 16S rRNA sequencing and metabolomic analysis using GC-MS. The study also used MPTP-induced PD mouse models to assess the protective effects of cholic acid on olfactory function and dopaminergic neurons.</p><p> </p><p>Results: The study found significant differences in nasal microbiota composition and metabolite profiles between PD patients and controls, with correlations to the severity of olfactory dysfunction. Specifically, the relative abundances of Corynebacterium, Dolosigranulum, Muribacter, and Moraxella were elevated in the PD group, while the abundances of Hydrogenophaga, Staphylococcus, Klebsiella, and Bacillus decreased. Metabolomic analysis revealed that cholic acid, octanal, hexadecanol, and phytol were significantly altered in PD patients compared to controls, with cholic acid showing potential as a diagnostic biomarker (AUC > 0.97). In MPTP-induced PD mouse models, cholic acid treatment significantly reduced latencies in detecting buried food pellets, and increased tyrosine hydroxylase (TH)-positive fluorescence intensity in the olfactory bulb and substantia nigra. However, cholic acid did not significantly ameliorate motor symptoms in PD mice, as assessed by the open field test, and did not prevent the loss of TH+ cells in the striatum.</p><p> </p><p>Conclusion: The findings highlight the interplay between the nasal microbiome, metabolome, and olfactory dysfunction in PD, suggesting that modulating metabolic pathways could be a promising therapeutic strategy. Future research should focus on larger sample sizes, longitudinal studies, and further validation of biomarkers and therapeutic targets to enhance the understanding and management of PD.</p>
2025-07-07 | MTBLS12692 | MetaboLights
Project description:<p><strong>PURPOSE:</strong> Olfactory dysfunction (OD) is a debilitating symptom frequently reported by patients with chronic rhinosinusitis (CRS) and it is associated with a dysregulated sinonasal inflammation. However, little information is available about the effect of the inflammation-related nasal microbiota and related metabolites on the olfactory function in these patients. Therefore, the current study aimed to investigate the nasal microbiota-metabolites-immune interactions and their role in the pathogenesis of OD in CRS patients.</p><p><strong>METHODS:</strong> 23 and 19 CRS patients with and without OD (NOD), respectively, were enrolled in the present study. The 'Sniffin' Sticks' was used to measure the olfactory function, while the metagenomic shotgun sequencing and the untargeted metabolomic profiling were performed to assess the differences in terms of the nasal microbiome and metabolome between the two groups. The levels of nasal mucus inflammatory mediators were investigated by a multiplex flow Cytometric Bead Array (CBA).</p><p><strong>RESULTS:</strong> A decreased diversity in the nasal microbiome from the OD group compared to the NOD group was evidenced. The metagenomic analysis revealed a significant enrichment of <em>Acinetobacter johnsonii</em> in the OD group, while <em>Mycoplasma arginini</em>, <em>Aeromonas dhakensis</em> and <em>Salmonella enterica</em> were significantly less represented (LDA value > 3, p < 0.05). The nasal metabolome profiles were significantly different between the OD and NOD groups (P < 0.05). The purine metabolism was the most significantly enriched metabolic subpathway in OD patients compared with NOD patients (P < 0.001). The expressions of IL-5, IL-8, MIP-1alpha, MCP-1 and TNF were statistically and significantly increased in the OD group (P < 0.05). All these data, including the dysregulation of the nasal microbiota, differential metabolites and elevated inflammatory mediators in OD patients demonstrated a clear interaction relationship.</p><p><strong>CONCLUSIONS:</strong> The disturbed nasal microbiota-metabolite-immune interaction networks may be implicated in the pathogenesis of OD in CRS patients and the underlying pathophysiological mechanisms need to be further investigated in future studies.</p>
2023-05-12 | MTBLS7584 | MetaboLights
Project description:The pathophysiology of post-infectious and idiopathic olfactory loss is still poorly delineated. Since proteins are key players in olfaction and technical advances including LC-MS/MS mass spectrometry give us the opportunity for detailed analysis of the nasal mucus proteome we aimed to undertake a comparative analysis of the olfactory cleft mucus proteome using mucus samples of the olfactory cleft in patients with idiopathic and postinfectious olfactory disorders versus healthy controls. The study was conceived as a pilot study and included 7 patients with idiopathic hyp- and anosmia, 7 patients with postinfectious hyp- and anosmia and 7 healthy controls. In total, 1117 different proteins were detected in at least 5 patients in at least one group. No significant different overall protein concentrations in patients compared to healthy controls (0.4614 µg/µL, SD=0.26273 vs. 0.5143 µg/µL, SD=3087; p=0.689) were found. Significant correlation regarding olfactory test results (TDI score) and protein concentrations (r=0.114, p=0.623) were either found. Results of this study did not show significant differences regarding the proteomic composition of the olfactory cleft mucus between patients suffering from postinfectious and idiopathic dysosmia versus healthy controls. Thus, central olfactory processing pathways may play a role in idiopathic and postinfectious olfactory disorders.
2018-12-10 | PXD009172 | Pride
Project description:SARS-CoV-2 infection causes a wide spectrum of clinical manifestations in human, and olfactory dysfunction represents as one of the most predictive and common symptoms in COVID-19 patients. Herein we demonstrate intranasal inoculation of SARS-CoV-2 induces robust viral replication in the olfactory epithelium (OE), not olfactory bulb (OB), resulting in transient olfactory dysfunction in humanized ACE2 mice. To decipher the underlying mechanism of the observed olfactory dysfunction in SARS-CoV-2 infected mice at the molecular level, RNA-Seq analyses of the OE and OB samples from SARS-CoV-2 infected mice were performed in comparison with that from the control animals.
2021-07-12 | GSE173186 | GEO
Project description:Background: The olfactory epithelium (OE) is one of the few sites where environmental pathogens can gain direct access to the brain. Despite this vulnerable arrangement, little is known about the protective mechanisms in the OE to prevent viral infection and subsequent entry into the brain. Methods: We systematically investigated acute responses in the olfactory mucosa (OM) upon exposure to vesicular stomatitis virus (VSV) by RNA-seq. VSVs were nasally inoculated into C57BL/6 mice. OM were dissected for gene expression analysis at different time points after viral inoculation. Interferon functions were determined by comparing viral gene expression in interferon (Ifn) receptor knockout (Ifnar1-/- and Ifnlr1-/-) with wildtype OM. Results: Antiviral responses were observed as early as 24hrs post viral exposure in the OM. Amongst the rapidly upregulated transcripts observed were specific type I as well as type III Ifns and interferon stimulated genes. Genetic analyses demonstrated that both type I and type III IFN signaling are required for the suppression of viral replication in the OM. Nasal IFNb1 or IFNl2 administration effectively reduces viral load in the OM. Conclusions: OE possesses innate ability to respond and suppress viral infection. Type I and type III IFNs actively participate in the OE’s antiviral functions. Nasal IFN application effectively blocks viral replication in the OE suggesting therapeutic potential against viral insult.
2023-07-03 | GSE154235 | GEO
Project description:SARS-CoV-2 infection causes a wide spectrum of clinical manifestations in human, and olfactory dysfunction represents as one of the most predictive and common symptoms in COVID-19 patients. However, the underlying mechanism how SARS-CoV-2 infection leads to olfactory disorders remains elusive. Herein we demonstrate intranasal inoculation of SARS-CoV-2 induces robust viral replication in the olfactory epithelium (OE), not olfactory bulb (OB), resulting in transient olfactory dysfunction in humanized ACE2 mice. The sustentacular cells and Bowman's gland cells in the OE were identified as the major target cells of SARS-CoV-2 before the invasion into olfactory sensory neurons. Remarkably, SARS-CoV-2 infection triggers massive cell death and immune cell infiltration, and directly impairs the uniformity of OE structure. Combined transcriptomic and quantitative proteomic analyses reveal the induction of antiviral and inflammatory responses, as well as the downregulation of olfactory receptor (OR) genes in the OE from the infected animals. Overall, our mouse model recapitulates the olfactory dysfunction in COVID-19 patients, and provides critical clues to understand the physiological basis for extrapulmonary manifestations of COVID-19.
2021-06-22 | PXD026854 |
Project description:<p>Sepsis, defined as life-threatening organ dysfunction caused by infection is difficult to distinguish clinically from infection or post-operative inflammation. We hypothesized that in a heterogeneous group of critically ill children, there would be different metabolic profiles between post-operative inflammation, bacterial and viral infection and infection with or without organ dysfunction. 1D 1H nuclear magnetic resonance spectra were acquired in plasma samples from critically ill children. We included children with bacterial (n = 25) and viral infection (n = 30) and controls (n = 58) (elective cardiac surgery without infection). Principal component analysis was used for data exploration and partial least squares discriminant analysis models for the differences between groups. Area under receiver operating characteristic curve (AUC) values were used to evaluate the models. Univariate analysis demonstrated differences between controls and bacterial and viral infection. There was excellent discrimination between bacterial and control (AUC = 0.94), and viral and control (AUC = 0.83), with slightly more modest discrimination between bacterial and viral (AUC = 0.78). There was modest discrimination (AUC = 0.73) between sepsis with organ dysfunction and infection with no organ dysfunction. In critically ill children, NMR metabolomics differentiates well between those with a post-operative inflammation but no infection, and those with infection (bacterial and viral), and between sepsis and infection.</p>
2020-11-19 | MTBLS563 | MetaboLights
Project description:Secondary bacterial pneumonia following influenza infection is a significant cause of mortality worldwide. Upper respiratory tract pneumococcal carriage is important as both determinants of disease and population transmission. The immunological mechanisms that contain pneumococcal carriage are well-studied in mice but remain unclear in humans. Loss of this control of carriage following influenza infection is associated with secondary bacterial pneumonia during seasonal and pandemic outbreaks. We used a human type 6B pneumococcal challenge model to show that carriage acquisition induces early degranulation of resident neutrophils and recruitment of monocytes to the nose. Monocyte function associated with clearance of pneumococcal carriage. Prior nasal infection with live attenuated influenza virus induced inflammation, impaired innate function and altered genome-wide nasal gene responses to pneumococcal carriage. Levels of the cytokine IP-10 promoted by viral infection at the time of pneumococcal encounter was positively associated with bacterial density. These findings provide novel insights in nasal immunity to pneumococcus and viral-bacterial interactions during co-infection.
2018-07-25 | GSE117580 | GEO
Project description:Nasal biopsies were collected from control and A-T patients prior to establishing olfactory neurosphere derived (ONS) cells. These cells were phenotyped using stem cell markers, a series of A-T cellular characteristics determined and cells differentiated into neuronal cells.
2013-01-10 | E-MTAB-1217 | biostudies-arrayexpress