Human lung metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB10129 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR240598.fastq.gz | Fastqsanger.gz | |||
| DRR240599.fastq.gz | Fastqsanger.gz | |||
| DRR240600.fastq.gz | Fastqsanger.gz | |||
| DRR240601.fastq.gz | Fastqsanger.gz | |||
| DRR240602.fastq.gz | Fastqsanger.gz |
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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: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.
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Project description:Influenza A virus (IAV) causes severe respiratory infections and alveolar epithelial damage resulting in acute respiratory distress syndrome (ARDS). Extracellular vesicles (EV) have been shown to mediate cellular crosstalk in inflammation by transfer of microRNAs. In this study, we found significant changes in the miRNA composition of EVs in the broncho-alveolar lavage fluid (BALF) from patients with IAV-induced ARDS. Among the nine significantly deregulated microRNAs, miR-17-5p was upregulated in patients` BALF and in EVs of IAV-infected lung epithelial cells (A549). In these cells, transfer of miR-17-5p strongly downregulated expression of the antiviral factor Mx1 and significantly enhanced IAV replication.
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Project description:Bronchoalveolar lavage fluid (BALF) collected from mice with and without the induction of Acute Respiratory Distress Syndrome (ARDS) and treated with engineered extracellular vesicles (EVs). BALF extracts were analyzed by LC-MS/MS performed in an 6545 Q-TOF LC/MS (AGILENT) using a Poroshell 120 SB-C18 reversed phase column (2.1 x 100 mm, 2.7 um). (NEGATIVE mode)
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Project description:Bronchoalveolar lavage fluid (BALF) collected from mice with and without the induction of Acute Respiratory Distress Syndrome (ARDS) and treated with engineered extracellular vesicles (EVs). BALF extracts were analyzed by LC-MS/MS performed in an 6545 Q-TOF LC/MS (AGILENT) using a Poroshell 120 SB-C18 reversed phase column (2.1 x 100 mm, 2.7 um)
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Project description:Bronchoalveolar lavage samples collected from lung transplant recipients. Numeric portion of sample name is an arbitrary patient ID and AxBx number indicates the perivascular (A) and bronchiolar (B) scores from biopsies collected on the same day as the BAL fluid was collected. Several patients have more than one sample in this series and can be determined by patient number followed by a lower case letter. Acute rejection state is determined by the combined A and B score - specifically, a combined AB score of 2 or greater is considered an acute rejection. Keywords = Bronchoalveolar lavage Keywords = lung transplant Keywords: other
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Project description:The Acute Respiratory Distress Syndrome (ARDS)/Acute Lung Injury (ALI) was described 30 years ago, yet the interaction between specific sets of genes involved in this syndrome remains incompletely understood. Keywords: disease state analysis
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Project description:Although respiratory distress is a common complication of severe malaria, little is known about the underlying molecular basis of lung dysfunction. Animal models have provided powerful insights into the pathogenesis of severe malaria syndromes such as cerebral malaria; however, no model of malaria-induced lung injury has been definitively established. This work used bronchoalveolar lavage (BAL), histopathology and gene expression analysis to examine the development of acute lung injury (ALI) in mice infected with Plasmodium berghei ANKA (PbA). BAL fluid of PbA-infected C57BL/6 mice revealed a significant increase in IgM and total protein prior to the development of cerebral malaria (CM), indicating disruption of the alveolar-capillary membrane barrier – the physiological hallmark of acute lung injury (ALI). In contrast to sepsis-induced ALI, BAL fluid cell counts remained constant with no infiltration of neutrophils. Histopathology showed septal inflammation without cellular transmigration into the alveolar spaces. Microarray analysis comparing malaria-induced ALI with sepsis-induced ALI identified several common gene ontology groups characterizing ALI in these models, including defense and immune response. Severity of malaria-induced ALI varied in a panel of inbred mouse strains, and development of ALI correlated with peripheral parasite burden but not CM susceptibility. CD36-/- mice, which have decreased parasite lung sequestration, were relatively protected from ALI. In summary, parasite burden and CD36-mediated sequestration in the lung are primary determinants of ALI in experimental murine malaria. Furthermore, differential susceptibility of mouse strains to malaria-induced ALI and CM indicate that distinct genetic determinants likely regulate susceptibility to these two important causes of malaria-associated morbidity and mortality. Keywords: Time course
2008-01-31 | GSE9497 | GEO
Project description:Bronchoalveolar lavage fluid (BALF) collected from mice with and without the induction of Acute Respiratory Distress Syndrome (ARDS) and treated with engineered extracellular vesicles (EVs). BALF extracts were analyzed by LC-MS/MS performed in an 6545 Q-TOF LC/MS (AGILENT) using a Poroshell 120 SB-C18 reversed phase column (2.1 x 100 mm, 2.7 um) (POS mode MS1 1E4, MS2 1E3)
2022-07-05 | MSV000089808 | GNPS
Project description:Rationale: The acute respiratory distress syndrome is refractory to pharmacological intervention. Inappropriate activation of alveolar neutrophils is believed to underpin this disease’s complex pathophysiology, yet these cells have been little studied. Objectives: To examine the functional and transcriptional profiles of patient blood and alveolar neutrophils compared to healthy volunteer cells, and define their sensitivity to phosphoinositide 3-kinase inhibition. Methods: Twenty three ventilated patients underwent bronchoalveolar lavage. Alveolar and blood neutrophil apoptosis, phagocytosis and adhesion molecules were quantified by flow cytometry, and oxidase responses by chemiluminescence. Cytokine and transcriptional profiling utilized multiplex and GeneChip arrays. Measurements and Main Results: Patient blood and alveolar neutrophils were distinct from healthy circulating cells, with increased CD11b and reduced CD62L expression, delayed apoptosis and constitutively primed oxidase responses. Incubating control cells with disease bronchoalveolar lavage recapitulated the aberrant functional phenotype and this could be reversed by phosphoinositide 3-kinase inhibitors. In contrast, the pro-survival phenotype of patient cells was recalcitrant to phosphoinositide 3-kinase inhibition. RNA transcriptomic analysis revealed modified immune, cytoskeletal and cell death pathways in patient cells, aligning closely to sepsis and burns data sets but not with phosphoinositide 3-kinase signatures. Conclusions: Acute respiratory distress syndrome blood and alveolar neutrophils display a distinct primed, pro-survival profile and transcriptional signature. The enhanced respiratory burst was phosphoinositide 3-kinase-dependent, but delayed apoptosis and the altered transcriptional profile were not. These unexpected findings cast doubt over the utility of phosphoinositide 3-kinase inhibition in acute respiratory distress syndrome and highlight the importance of evaluating novel therapeutic strategies in patient-derived cells.
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