Vagus nerve inflammation in COVID-19
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA977669 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24765648_1.fastq.gz | Fastqsanger.gz | |||
| SRR24765648_2.fastq.gz | Fastqsanger.gz | |||
| SRR24765649_1.fastq.gz | Fastqsanger.gz | |||
| SRR24765649_2.fastq.gz | Fastqsanger.gz | |||
| SRR24765650_1.fastq.gz | Fastqsanger.gz |
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Project description:To find inflammatory signatures in post mortem vagus nerves of COVID-19 patients in comparisin to non-infected controls.
2023-08-21 | GSE233732 | GEO
Project description:Because the vagus nerve is implicated in control of inflammation, we investigated if brain death causes impairment of the parasympathetic nervous system, hence contributing to inflammation. Brain death (BD) was induced in rats. Anaesthetised ventilated rats (NBD) served as control. Heart rate variability (HRV) was assessed by ECG. The vagus nerve was electrically stimulated (BD+STIM) during BD. Intestine, kidney, heart and liver were harvested after 6h. Affymetrix chip- analysis was performed on intestinal RNA. Quantitative PCR was performed on all organs. Serum was collected to assess TNFα concentrations. Renal transplantations were performed to address the influence of vagus nerve stimulation on graft outcome. HRV was significantly lower in BD animals. Vagus nerve stimulation inhibited the increase in serum TNFα concentrations and resulted in down-regulation of a multiplicity of pro-inflammatory genes in intestinal tissue. In renal tissue vagal stimulation significantly decreased the expression of E-selectin, IL1β and ITGA6. Renal function was significantly better in recipients that received a graft from a BD+STIM donor. Our study demonstrates impairment of the parasympathetic nervous system during BD and inhibition of serum TNFα through vagal stimulation. Vagus nerve stimulation variably affected gene expression in donor organs and improved renal function in recipients. Gene expression in brain dead (BD) induced rat (with and without vagal stimulation) was compared with that of Non brain-dead ventilated control (NBD)
2010-05-19 | E-GEOD-16483 | biostudies-arrayexpress
Project description:Because the vagus nerve is implicated in control of inflammation, we investigated if brain death causes impairment of the parasympathetic nervous system, hence contributing to inflammation. Brain death (BD) was induced in rats. Anaesthetised ventilated rats (NBD) served as control. Heart rate variability (HRV) was assessed by ECG. The vagus nerve was electrically stimulated (BD+STIM) during BD. Intestine, kidney, heart and liver were harvested after 6h. Affymetrix chip- analysis was performed on intestinal RNA. Quantitative PCR was performed on all organs. Serum was collected to assess TNFα concentrations. Renal transplantations were performed to address the influence of vagus nerve stimulation on graft outcome. HRV was significantly lower in BD animals. Vagus nerve stimulation inhibited the increase in serum TNFα concentrations and resulted in down-regulation of a multiplicity of pro-inflammatory genes in intestinal tissue. In renal tissue vagal stimulation significantly decreased the expression of E-selectin, IL1β and ITGA6. Renal function was significantly better in recipients that received a graft from a BD+STIM donor. Our study demonstrates impairment of the parasympathetic nervous system during BD and inhibition of serum TNFα through vagal stimulation. Vagus nerve stimulation variably affected gene expression in donor organs and improved renal function in recipients.
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Project description:In France, new cancer cases keep on increasing with around 150 000 deaths yearly. Cancer therapy research is constantly evolving. Indeed, several studies explore new treatments or their combination with conventional cancer treatments. But, at the same time, complementary and alternative medicines, as osteopathy, remain little explored upon their role in the combination with conventional therapy.
Several studies showed indirect interaction between vagus nerve and cancer. Firstly, vagus nerve regulates homeostasis and immunity by reducing systemic inflammation while maintaining local inflammation and antitumor effects. Secondly, vagus nerve stimulation increases Heart Rate Variability (HRV). Moreover, a higher HRV is associated with an improvement of vital prognosis in cancer patients. Vagus nerve could be stimulated by noninvasive osteopathic manipulations.
This prospective, monocentric and randomized study is a collaboration between the Centre Hospitalier d’Avignon and the Institut de Formation en Ostéopathie du Grand Avignon. It focuses on using noninvasive osteopathic mobilizations to stimulate vagus nerve. Indeed, this study aims to evaluate effects of vagus nerve osteopathic stimulations on HRV in patients with lung cancer, colorectal cancer, Non Hodgkin Lymphoma or Multiple Myeloma. More specifically, this study will tell us whether vagus nerve noninvasive osteopathic stimulations induce increase of HRV associated with a decrease of systemic inflammation and an improvement of patient’s quality of life.
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Project description:Although most SARS-CoV-2-infected individuals experience mild COVID-19, some patients suffer from severe COVID-19, which is accompanied by acute respiratory distress syndrome and systemic inflammation. To identify factors driving severe progression of COVID-19, we performed single-cell RNA-seq using peripheral blood mononuclear cells (PBMCs) obtained from healthy donors, patients with mild or severe COVID-19, and patients with severe influenza. Patients with COVID-19 exhibited hyper-inflammatory signatures across all types of cells among PBMCs, particularly upregulation of the TNF/IL-1beta-driven inflammatory response as compared to severe influenza. In classical monocytes from patients with severe COVID-19, type I IFN response co-existed with the TNF/IL-1beta-driven inflammation, and this was not seen in patients with milder COVID-19 infection. Based on this, we propose that the type I IFN response exacerbates inflammation in patients with severe COVID-19 infection.
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Project description:Purpose: To decipher the mechanisms responsible for the protective function of vagus nerve stimulation. Methods: Blood was collected from Control and Treated patients followed by isolation of PBMC'S. Total RNA was extracted and RNA sequencing was done following standard protocols Results: Detailed analysis of the transcriptomic data show that anti-inflammatory responses were upregulated in the treated samples. Conclusions: This study showed the protective role of vagus nerve stimulation in epilepsy patients.
2023-03-01 | GSE210043 | GEO
Project description:Post-acute sequelae of COVID-19 (PASC) represent an emerging global crisis. However, quantifiable risk-factors for PASC and their biological associations are poorly resolved. We executed a deep multi-omic, longitudinal investigation of 309 COVID-19 patients from initial diagnosis to convalescence (2-3 months later), integrated with clinical data, and patient-reported symptoms. We resolved four PASC-anticipating risk factors at the time of initial COVID-19 diagnosis: type 2 diabetes, SARS-CoV-2 RNAemia, Epstein-Barr virus viremia, and specific autoantibodies. In patients with gastrointestinal PASC, SARS-CoV-2-specific and CMV-specific CD8+ T cells exhibited unique dynamics during recovery from COVID-19. Analysis of symptom-associated immunological signatures revealed coordinated immunity polarization into four endotypes exhibiting divergent acute severity and PASC. We find that immunological associations between PASC factors diminish over time leading to distinct convalescent immune states. Detectability of most PASC factors at COVID-19 diagnosis emphasizes the importance of early disease measurements for understanding emergent chronic conditions and suggests PASC treatment strategies.
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Project description:The severity of COVID-19 is linked to excessive inflammation. Neutrophils represent a critical arm of the innate immune response and are major mediators of inflammation, but their role in COVID-19 pathophysiology remains poorly understood. We conducted transcriptomic profiling of neutrophils obtained from patients with mild and severe COVID-19, as well as from non-infected healthy controls. Additionally, low-density granulocytes (LDGs) from patients with severe COVID-19 were included to understand their unique role. Transcriptomic analysis of polymorphonuclear cells (PMNs), consisting mainly of mature neutrophils, revealed a striking type I interferon (IFN-I) gene signature in severe COVID-19 patients, contrasting with mild COVID-19 and healthy controls. LDGs from severe COVID-19 patients exhibited an immature neutrophil phenotype and lacked this IFN-I signature. These findings underscore the crucial role of neutrophil inflammasomes in driving inflammation during severe COVID-19. The study provides insights into the pathological mechanisms of severe COVID-19 and highlights potential targets for therapeutic intervention.
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Project description:The ongoing SARS-CoV-2 pandemic has resulted in over 6.3 million deaths and 560 million COVID-19 cases worldwide. Clinical management of hospitalised patients is complex due to the heterogeneous course of COVID-19. Low-dose radiotherapy (LD-RT) is known to dampen localised chronic inflammation, and has been suggested to be used to reduce lung inflammation in COVID-19 patients. However, it is unknown whether SARS-CoV-2 alters the radiation response and associated radiation exposure related risk. We generated gene expression profiles from circulating leukocytes of hospitalised COVID-19 patients and healthy donors. The p53 signalling pathway was found to be dysregulated, with mRNA levels of p53, ATM and CHK2 being lower in COVID-19 patients. Several key p53 target genes involved in cell cycle arrest, apoptosis and p53 feedback inhibition were up-regulated in COVID-19 patients, while other p53 target genes were downregulated. This dysregulation has functional consequences as the transcription of p53-dependant genes (CCNG1, GADD45A, DDB2, SESN1, FDXR, APOBEC) was reduced 24 h after X-ray exposure ex-vivo to both low (100 mGy) or high (2 Gy) doses. In conclusion, SARS-CoV-2 infection affects a DNA damage response that may modify radiation-induced health risks in exposed COVID-19 patients.
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