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Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19

ABSTRACT: Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19

PROVIDER: PRJNA705880 | ENA |

REPOSITORIES: ENA

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Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19 (bulkRNA-seq)

Project description:Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19 (bulkRNA-seq)

| PRJNA705883 | ENA

Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19 (scRNA-seq)

Project description:Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19 (scRNA-seq)

| PRJNA705884 | ENA

Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19 (scRNA-seq)

Project description:We preformed a systems biological assessment of lower respiratory tract host immune responses and microbiome dynamics in COVD-19 patients, using bulk RNA-sequencing, single-cell RNA sequencing, and techniques, and microbiome analysis. Are focus was on differential gene expression in severe COVID-19 patients who developed ventilator associated pneumonia (VAP) during their course versus severe COVID-19 patients who did not develop VAP. We found early impairment in antibacterial immune signaling in patients two or more weeks prior to the development of VAP, compared to COVID-19 patients who did not develop VAP. There was no signficant difference in viral load, but an association of disruption in lung microbiome by alpha and beta diversity metrics was also found.

2021-03-03 | GSE168018 | GEO

Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19 (bulkRNA-seq)

2021-03-03 | GSE168017 | GEO

Impaired antibacterial immune signaling and changes in the lung microbiome precedes secondary bacterial pneumonia in COVID-19

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-03-03 | GSE168019 | GEO

Microbial Dynamics and Pulmonary Immune Responses in COVID-19 Secondary Bacterial Pneumonia

Project description:Metatranscriptomic analysis identifies a state of pathogen dominance and suppressed pulmonary immune signaling in critically ill COVID-19 patients with secondary bacterial pneumonia.

2024-09-20 | GSE246795 | GEO

Type II interferon-dependent antibacterial defense in the lungs is compromised in diabetes

Project description:Diabetes mellitus is associated with an increased risk of pneumonia, which is often caused by so-called typical and atypical pathogens including Streptoccocus pneumoniae and Legionella pneumophila, respectively. Here, we employed a varity of mouse models to investigate how diabetes influences pulmonary antibacterial immunity. Following intranasal infection with Streptoccocus pneumoniae or Legionella pneumphila, type 2 diabetic and prediabetic mice had higher bacterial loads in their lungs as compared to control animals. Single cell RNA sequencing, flow cytometry, and functional analyses revealed a compromised type II IFN (IFNg) production by natural killer cells in diabetic and prediabetic mice, which was linked to reduced IL-12 production by CD103+ dendritic cells. Treatment with IFNg rescued antibacterial defense against L. pneumophila but not against S. pneumoniae in diabetic animals, although impaired production of IFNg also contributed to the compromised anti-pneumococcal resistance in diabetic mice. These findings uncover a mechanism that could help to explain why type 2 diabetes predisposes to pneumonia. We establish proof of concept for host-directed treatment strategies to reinforce compromised IFNg-mediated antibacterial defense against atypical lung pathogens.

2024-11-19 | GSE270694 | GEO

RNA-sequencing of primary and secondary bacterial pneumonia

Project description:RNA-sequencing of primary and secondary bacterial pneumonia

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RNA-sequencing of primary and secondary bacterial pneumonia

Project description:Influenza infection is substantially worsened by the onset of secondary pneumonia caused by bacteria such as methicillin-resistant Staphylococcus aureus (MRSA). The bidirectional interaction between the influenza-injured lung microenvironment and MRSA is poorly understood. By conditioning MRSA ex vivo in bronchoalveolar lavage fluid collected from mice at various timepoints of influenza infection, we found that the influenza-injured lung microenvironment dynamically induces MRSA to increase cytotoxin expression while decreasing metabolic pathways. LukAB, a SaeRS two-component system dependent cytotoxin, is particularly important to the severity of post-influenza MRSA pneumonia. LukAB’s activity is likely shaped by the post-influenza lung microenvironment, as LukAB binds to (and is activated by) heparan sulfate (HS) oligosaccharide sequences shed from the epithelial glycocalyx after influenza. Our findings indicate that post-influenza MRSA pneumonia is shaped by bidirectional host-pathogen interactions: host injury triggers changes in bacterial expression of toxins, the activity of which may be shaped by host-derived HS fragments.

2022-11-29 | GSE199707 | GEO

Antibiotic use during influenza infection augments lung eosinophils that impair lung immunity against secondary bacterial pneumonia

Project description:A leading cause of morbidity and mortality during influenza infection is the development of a secondary bacterial pneumonia, which is appropriately treated with antibiotics. In the absence of a bacterial superinfection, prescribing antibiotics is not indicated but has nevertheless become a common clinical practice for those presenting with a respiratory viral illness. We found that antibiotic use during an antecedent influenza infection impaired the lung innate immunologic defenses toward a secondary challenge with methicillin-resistantStaphylococcus aureus(MRSA). The antibiotics perturbed the gut microbiome causing a fungal dysbiosis that drives an increase in lung eosinophils. We also demonstrate eosinophils, through the release of major basic protein, impair macrophage ability to clear MRSA. Moreover, we provide clinical evidence that eosinophils positively correlate with antibiotic use and worsened outcomes in patients hospitalized for viral infections. Altogether, our work establishes a counterproductive effect of antibiotic treatment during influenza infection that have negative immunologic consequences in the lungs thereby increasing the risk of developing a secondary bacterial infection.

2024-08-21 | GSE259429 | GEO

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