Human gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB13936 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A Study to Elucidate the Gastrointestinal mucosal damage in Patients with COVID-19
| PRJEB54760 | ENA
Project description:In this prospective observational cohort study, we found transcriptional evidence that persistent immune dysfunction was associated with 28-day mortality in both COVID-19 and non-COVID-19 septic patients. COVID-19 patients had an early antiviral response but became indistinguishable on a gene expression level from non-COVID-19 sepsis patients a week later. Early treatment of COVID-19 and non-COVID-19 sepsis ICU patients should focus on pathogen control, but both patient groups also require novel immunomodulatory treatments, particularly later during ICU hospitalization, independent of admission diagnosis. Some T1 samples were uploaded in GSE185263 and were not re-uploaded in this series.
2023-03-24 | GSE222393 | GEO
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections cause coronavirus disease 2019 (COVID-19) and are associated with inflammation and coagulopathy and high incidence of thrombosis. Myeloid cells (Mϕ) help coordinate the initial immune response in COVID-19. Although we appreciate that Mϕ lie at the nexus of inflammation and thrombosis, the mechanisms that unite the two in COVID-19 remain largely unknown. In this study, we employed systems biology approaches including proteomics, transcriptomics, and mass cytometry to define the circulating proteome and circulating immune cell phenotypes in subjects with COVID-19. In a cohort of COVID-19 subjects (n=35), circulating markers of inflammation (CCL23, IL-6) and vascular dysfunction (ACE2, tissue factor [TF]) were elevated in subjects with severe compared with mild COVID-19. Additionally, although the total white blood cell (WBC) counts were similar between COVID-19 groups, CD14+ monocytes from severe COVID-19 subjects expressed more TF. At baseline, transcriptomics demonstrated increased IL-6, CCL3, ACOD1, C5AR1, C5AR2, and TF in severe COVID-19 subjects compared with controls. Using “stress” transcriptomics, we found that circulating immune cells from severe COVID-19 subjects had evidence of profound immune paralysis with greatly reduced transcriptional activation and release of inflammatory markers in response to Toll-like receptor (TLR) activation. Finally, sera from severe (but not mild) COVID-19 subjects activated human monocytes and induced TF expression. Taken together, these observations further elucidate the pathological mechanisms that underlie immune dysfunction and coagulation abnormalities in COVID-19, contributing to our growing understanding of SARS-CoV-2 infections that could also be leveraged to develop novel diagnostic and therapeutic strategies.
2024-01-23 | GSE247186 | GEO
Project description:The adult data set. The pathogenesis of multi-organ dysfunction associated with severe acute SARS-CoV-2 infection remains poorly understood. Endothelial damage and microvascular thrombosis have been identified as drivers of COVID-19 severity, yet the mechanisms underlying these processes remain elusive. A multiomics approach identified alterations in analytes associated with fluid shear stress-responsive pathways in critically ill COVID-19 adults as compared to non-COVID critically ill adults.
2023-03-06 | PXD040438 | Pride
Project description:This prospective observational study conducted at Osaka University Graduate School of Medicine aimed to compare host responses in sepsis and COVID-19 patients by analyzing mRNA and miRNA profiles. They included 22 sepsis patients, 35 COVID-19 patients, and 15 healthy subjects. Sepsis was diagnosed using Sepsis-3 criteria, while COVID-19 was confirmed through SARS-CoV-2 RT-PCR testing and chest CT scans for pneumonia assessment. For RNA sequencing, 14,500 mRNAs, 1121 miRNAs, and 2556 miRNA-targeted mRNAs were available for analysis in sepsis patients. Numbers of genes showing upregulated:downregulated gene expression (false discovery rate <0.05, |log2 fold change| >1.5) were 256:2887 for mRNA, 53:5 for miRNA, and 49:2507 for miRNA-targeted mRNA. Similarly, in COVID-19 patients, 14,500 mRNAs, 1121 miRNAs, and 327 miRNA-targeted mRNAs were analyzed, with numbers of genes exhibiting upregulated:downregulated gene expression of 672:1147 for mRNA, 3:4 for miRNA, and 165:162 for miRNA-targeted mRNA. Sepsis patients had a greater number of upregulated and downregulated genes and pathways compared to COVID-19 patients, indicating a dynamic change in gene expression and pathway activation in sepsis.
2024-08-28 | GSE243218 | GEO
Project description:This prospective observational study conducted at Osaka University Graduate School of Medicine aimed to compare host responses in sepsis and COVID-19 patients by analyzing mRNA and miRNA profiles. They included 22 sepsis patients, 35 COVID-19 patients, and 15 healthy subjects. Sepsis was diagnosed using Sepsis-3 criteria, while COVID-19 was confirmed through SARS-CoV-2 RT-PCR testing and chest CT scans for pneumonia assessment. For RNA sequencing, 14,500 mRNAs, 1121 miRNAs, and 2556 miRNA-targeted mRNAs were available for analysis in sepsis patients. Numbers of genes showing upregulated:downregulated gene expression (false discovery rate <0.05, |log2 fold change| >1.5) were 256:2887 for mRNA, 53:5 for miRNA, and 49:2507 for miRNA-targeted mRNA. Similarly, in COVID-19 patients, 14,500 mRNAs, 1121 miRNAs, and 327 miRNA-targeted mRNAs were analyzed, with numbers of genes exhibiting upregulated:downregulated gene expression of 672:1147 for mRNA, 3:4 for miRNA, and 165:162 for miRNA-targeted mRNA. Sepsis patients had a greater number of upregulated and downregulated genes and pathways compared to COVID-19 patients, indicating a dynamic change in gene expression and pathway activation in sepsis.
2024-08-28 | GSE243217 | GEO
Project description:The coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains to spread worldwide. COVID-19 is characterized by the striking high mortality in elderly; however, its mechanistic insights remain unclear. Systemic thrombosis has been highlighted in the pathogenesis of COVID-19, and lung microangiopathy in association with endothelial cells (ECs) injury has been reported by post-mortem analysis of the lungs. Here, we experimentally investigated the SARS-CoV-2 infection in cultured human ECs, and performed a comparative analysis for post-infection molecular events using early passage and replicative senescent ECs. We found that; 1) SARS-CoV-2 infects ECs but does not replicate and disappears in 72 hours without causing severe cell damage, 2) Senescent ECs are highly susceptible to SARS-CoV-2 infection, 3) SARS-CoV-2 infection alters various genes expression, which could cause EC dysfunctions, 4) More genes expression is affected in senescent ECs by SARS-CoV-2 infection than in early passage ECs, which might causes further exacerbated dysfunction in senescent ECs. These data suggest that sustained EC dysfunctions due to SARS-CoV-2 infection may contribute to the microangiopathy in the lungs, leading to deteriorated inflammation and thrombosis in COVID-19. Our data also suggest a possible causative role of EC senescence in the aggravated disease in elder COVID-19 patients.
2023-05-01 | GSE206677 | GEO
Project description:Coronavirus disease 2019 (COVID-19) is associated with serious cardiovascular complications, including myocarditis, thrombosis, and dysregulated hemodynamic responses. The mechanism(s) underlying these disease manifestations are incompletely understood. Given a critical role for pericytes in supporting endothelial cell health and maintaining vascular integrity, we hypothesized that infection of pericytes could explain some of the cardiovascular complications of COVID-19. Here, we present evidence of SARS-CoV-2 infection in cardiac pericytes in patients with COVID-19 myocarditis. We show that cardiac pericytes are permissive to SARS-CoV-2 infection in organotypic slice and primary cell cultures. SARS-CoV-2 enters cardiac pericytes through an ACE2 and endosomal-dependent mechanism. Consequences of cardiac pericyte infection include upregulation of inflammatory chemokine and cytokine expression, type I interferon signaling, mediators of endothelial constriction, and cell death. Collectively, these data demonstrate that human cardiac pericytes are susceptible to SARS-CoV-2 infection and suggest a possible role for pericyte infection in the pathogenesis of COVID-19.
2022-08-31 | GSE183850 | 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.
2022-02-01 | E-MTAB-10129 | biostudies-arrayexpress
Project description:The rapid development of safe and effective treatments for COVID-19 had become a top priority to fight against this spreading pandemic worldwide in 2019. 20%–30% of COVID-19 patients experience severe cardiovascular damage, patients with pre-existing heart complications are more likely to develop severe illness and have higher risk of death compared with patients without co-morbidities. In such a context, whether the repurposed drugs are at risk of inducing heart damage to COVID-19 patients remains unclear. Here, we demonstrated that four antiviral drugs, including apilimod, remdesivir, ritonavir, and lopinavir, exhibit cardiotoxicity at clinically relevant doses. RNA-seq analysis revealed that human pluripotent stem cell-derived cardiomyocytes (hCMs) treated by each drug had significantly different expression profiles when compared with the untreated control. The expression of genes that regulate cardiomyocyte function, such as sarcomere organization and ion hemostasis, was significantly altered after drug treatment. These results not only warrant caution and careful monitoring when prescribing the above-mentioned drugs in patients, but also provide a valuable platform for understanding the molecular mechanism underlined the toxic effects of these prospective drugs and for protective agent discovery.
2023-11-15 | GSE247541 | GEO