91c03c12-be38-41cb-9205-d5f07fc6014b - samples
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ABSTRACT:
PROVIDER: EGAD00001008161 | EGA |
REPOSITORIES: EGA
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Project description:We performed single-cell RNA-sequencing of cells in the bronchoalveolar lavage (BAL) fluid of severe COVID-19. In addition, we performed single-cell RNA-sequencing of SARS-CoV-2 stimulated classical blood monocytes. This study provides detailed insights into the alveolar macrophage response to SARS-CoV-2 infection and reveals a profibrotic macrophage response in severe COVID-19 patients.
| EGAD00001006827 | EGA
Project description:As many as 10–30% of the nearly 750 million survivors of COVID-19 develop persistent symptoms that define the post-acute sequelae of COVID-19 (PASC) syndrome. To understand the molecular basis of this syndrome, we combined a machine learning based analysis of lung computed tomography (CT) with flow cytometry and single cell RNA-sequencing analysis of bronchoalveolar lavage fluid and nasal curettage samples in a cohort of thirty-five patients with respiratory symptoms and radiographic abnormalities more than 90 days after infection with COVID-19. CT images from patients with PASC revealed primarily fibrotic abnormalities involving 73 +/- 28% of the lung, most of which improved on subsequent imaging. The presence of profibrotic monocyte-derived alveolar macrophages in BAL fluid was significantly associated with increased levels of alveolar cytokines and fibrotic abnormalities on CT. Persistent infection with SARS-CoV-2 was identified in 6 patients and secondary bacterial or viral infections in two others. These findings suggest persistent alveolar inflammation characterized by the ongoing recruitment of monocyte derived alveolar macrophages is associated with fibrotic CT changes in some COVID-19 survivors with implications for diagnosis and therapy.
2024-05-12 | GSE232627 | GEO
Project description:As many as 10–30% of the nearly 750 million survivors of COVID-19 develop persistent symptoms that define the post-acute sequelae of COVID-19 (PASC) syndrome. To understand the molecular basis of this syndrome, we combined a machine learning based analysis of lung computed tomography (CT) with flow cytometry and single cell RNA-sequencing analysis of bronchoalveolar lavage fluid and nasal curettage samples in a cohort of thirty-five patients with respiratory symptoms and radiographic abnormalities more than 90 days after infection with COVID-19. CT images from patients with PASC revealed primarily fibrotic abnormalities involving 73 +/- 28% of the lung, most of which improved on subsequent imaging. The presence of profibrotic monocyte-derived alveolar macrophages in BAL fluid was significantly associated with increased levels of alveolar cytokines and fibrotic abnormalities on CT. Persistent infection with SARS-CoV-2 was identified in 6 patients and secondary bacterial or viral infections in two others. These findings suggest persistent alveolar inflammation characterized by the ongoing recruitment of monocyte derived alveolar macrophages is associated with fibrotic CT changes in some COVID-19 survivors with implications for diagnosis and therapy.
2024-05-12 | GSE232623 | GEO
Project description:As many as 10–30% of the nearly 750 million survivors of COVID-19 develop persistent symptoms that define the post-acute sequelae of COVID-19 (PASC) syndrome. To understand the molecular basis of this syndrome, we combined a machine learning based analysis of lung computed tomography (CT) with flow cytometry and single cell RNA-sequencing analysis of bronchoalveolar lavage fluid and nasal curettage samples in a cohort of thirty-five patients with respiratory symptoms and radiographic abnormalities more than 90 days after infection with COVID-19. CT images from patients with PASC revealed primarily fibrotic abnormalities involving 73 +/- 28% of the lung, most of which improved on subsequent imaging. The presence of profibrotic monocyte-derived alveolar macrophages in BAL fluid was significantly associated with increased levels of alveolar cytokines and fibrotic abnormalities on CT. Persistent infection with SARS-CoV-2 was identified in 6 patients and secondary bacterial or viral infections in two others. These findings suggest persistent alveolar inflammation characterized by the ongoing recruitment of monocyte derived alveolar macrophages is associated with fibrotic CT changes in some COVID-19 survivors with implications for diagnosis and therapy.
2024-05-12 | GSE232616 | GEO
Project description:Hyperinflammation contributes to lung injury and subsequent acute respiratory distress syndrome (ARDS) with high mortality in severe COVID-19. To understand the underlying mechanisms, we investigated the role of the lung-specific immune response. Here we profiled lymphocytes and myeloid cells in the bronchoalveolar lavage (BAL) fluid and blood of COVID-19 patients. By tracking T cell clones across tissues, we identified clonally expanded tissue-resident memory-like Th17 cells (Trm17 cells) in the lung even after viral clearance. These Trm17 cells are characterized by a potentially pathogenic cytokine profile with expression of IL17A and CSF2 (GM-CSF). Interactome analysis revealed that Trm17 cells interact with macrophages and cytotoxic CD8+ T cells, which have been associated with disease severity and lung damage. High IL-17A and GM-CSF protein levels in the serum of COVID-19 patients correlated with severe clinical course. This study suggests pulmonary Trm17 cells as one of the orchestrators of the hyperinflammation in severe COVID-19 and that these cells and their cytokines, such as GM-CSF, are promising biomarkers and potential targets for a COVID-19 therapy.
2021-02-20 | GSE167118 | GEO
Project description:Immune characteristics associated with Coronavirus Disease-2019 (COVID-19) severity are currently unclear. We characterized bronchoalveolar lavage fluid (BALF) immune cells from patients with varying severity of COVID-19 disease and from healthy subjects using single-cell RNA-sequencing. Proinflammatory monocyte-derived macrophages were abundant in the BALF from severe COVID-9 patients. Moderate cases were characterized by the presence of highly clonally expanded tissue-resident CD8+ T cells. This atlas of the bronchoalveolar immune-microenvironment suggests potential mechanisms underlying pathogenesis and recovery in COVID-19.
2020-04-22 | GSE145926 | GEO
Project description:COVID-19-associated pulmonary aspergillosis (CAPA) is a frequent, severe superinfection with the fungus Aspergillus affecting critically ill COVID-19 patients. The pathophysiology of this infection is still largely unknown. We performed an explorative study by performing single-cell RNA sequencing (scRNA-seq) on 43 bronchoalveolar lavage (BAL) fluid samples from 39 mechanically ventilated COVID-19 patients.
| EGAS00001007556 | EGA
Project description:Some patients infected with Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) develop severe pneumonia and the acute respiratory distress syndrome (ARDS). Distinct clinical features in these patients have led to speculation that the immune response to virus in the SARS-CoV-2-infected alveolus differs from other types of pneumonia. We collected bronchoalveolar lavage fluid samples from 88 patients with SARS-CoV-2-induced respiratory failure and 211 patients with known or suspected pneumonia from other pathogens and subjected them to flow cytometry and bulk transcriptomic profiling. We performed single-cell RNA-seq on 10 bronchoalveolar lavage fluid samples collected from patients with severe COVID-19 within 48 hours of intubation. In the majority of patients with SARS-CoV-2 infection, the alveolar space was persistently enriched in T cells and monocytes. Bulk and single-cell transcriptomic profiling suggested that SARS-CoV-2 infects alveolar macrophages, which in turn respond by producing T cell chemoattractants. These T cells produce interferon-gamma to induce inflammatory cytokine release from alveolar macrophages and further promote T cell activation. Collectively, our results suggest that SARS-CoV-2 causes a slowly-unfolding, spatially-limited alveolitis in which alveolar macrophages harboring SARS-CoV-2 and T cells form a positive feedback loop that drives persistent alveolar inflammation.
2020-08-05 | GSE155249 | GEO
Project description:Proteomic analysis of bronchoalveolar lavage fluid in COVID-19 patients
2020-10-20 | PXD022085 |
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel viral pathogen that causes a clinical disease called coronavirus disease 2019 (COVID-19). Approximately 20% of infected patients experience a severe manifestation of the disease, causing bilateral pneumonia and acute respiratory distress syndrome. Severe COVID-19 patients also have a pronounced coagulopathy with approximately 30% of patients experiencing thromboembolic complications. However, the cellular etiology driving the coagulopathy remains unknown. Here, we explore whether the prominent neutrophilia seen in severe COVID-19 patients contributes to inflammation-associated coagulation. We found in severe patients the emergence of a CD16Int low-density inflammatory band (LDIB) neutrophil population that trends over time with changes in disease status. These cells demonstrated spontaneous neutrophil extracellular trap (NET) formation, higher phagocytic capacity, enhanced cytokine production, and associated clinically with D-dimer, ferritin, and systemic IL-6 and TNF-α levels. Strikingly, LDIB neutrophils are the major immune cells within the bronchoalveolar lavage (BAL) fluid with increased CXCR3 and loss of CD44 and CD38 expression. We conclude that the LDIB subset contributes to COVID- 19-associated coagulopathy (CAC) and systemic inflammation and could be used as an adjunct clinical marker to monitor disease status and progression. Identifying patients who are trending towards LDIB crisis and implementing early, appropriate treatment could improve all-cause mortality rates for severe COVID-19 patients.
2021-07-20 | GSE154311 | GEO