Neutrophil Transcriptomics During Pneumonia
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ABSTRACT:
PROVIDER: PRJNA714893 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE32105: Expression data from mouse livers lacking STAT3 and RelA during pneumonia GSE35513: Expression data from mouse livers lacking NF-kappaB RelA (p65) during pneumonia GSE35514: Expression data from mouse livers lacking STAT3 during pneumonia GSE35515: Expression data from mouse livers expressing or lacking Cre recombinase during pneumonia Refer to individual Series
2012-02-16 | E-GEOD-35516 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-03-06 | GSE169007 | GEO
Project description:Community acquired pneumonia (CAP) is a leading cause of hospitalistion and is associated with high mortality and morbidity. Neutrophils from CAP donors display altered functions, and these altered functions are associated with adverse outcomes. We undertook an oberservational study of CAP in frail older adults and age matched controls to determine drivers of neutrophil dysfunction.
2024-12-10 | GSE261559 | GEO
Project description:Oncostatin M (OSM) is an IL-6 family cytokine that is necessary for neutrophil recruitment in pneumonia by inducing STAT3-dependent production of CXCL5. We used microarrays to identify additional pathways affected by OSM neutralization in the lungs during pneumonia.
2021-03-08 | GSE155283 | GEO
Project description:Pneumonia caused by Streptococcus pneumoniae is a leading cause of death worldwide, and bacterial resistance to antimicrobial drugs has become a major issue. A growing body of evidence indicates that the successful treatment of bacterial infections results from synergy between antibiotic-mediated direct antibacterial activity and the host’s immune defenses. However, the mechanisms underlying the protective immune responses induced by amoxicillin (a β-lactam antibiotic used as the first-line treatment of S. pneumoniae infections) have not been characterized. A better understanding of amoxicillin’s effects on host-pathogen interactions might facilitate the development of other treatment options. Given the crucial role of neutrophils in the control of S. pneumoniae infections, we decided to investigate amoxicillin’s impact on neutrophil development in a mouse model of pneumococcal superinfection. Although a single therapeutic dose of amoxicillin prevented local and systemic inflammatory responses, it did not impair the emergency granulopoiesis triggered in the bone marrow by S. pneumoniae. Importantly, treatment of pneumonia with amoxicillin was associated with a greater mature neutrophil count in the bone marrow; these neutrophils had specific transcriptomic and proteomic profiles. Furthermore, amoxicillin-conditioned, mature neutrophils in the bone marrow had a less activated phenotype and might be rapidly mobilized in peripheral tissues in response to systemic inflammation. Thus, by revealing a novel effect of amoxicillin on the development and functions of bone marrow neutrophils during Streptococcus pneumoniae pneumonia, our findings provide new insights into the impact of amoxicillin treatment on host immune responses.
2023-10-09 | PXD042496 | Pride
Project description:Pulmonary innate immunity is required for host defense; however, excessive neutrophil inflammation can cause life-threatening acute lung injury. B lymphocytes can be regulatory, yet little is known about peripheral transitional IgM+ B cells in terms of regulatory properties. Using single cell RNA sequencing, we discovered eight IgM+ B cell subsets with unique gene regulatory networks in the lung circulation dominated by transitional type 1 (T1B) and 2 (T2B) B cells. Lung intravital confocal microscopy revealed that T2B marginate in the pulmonary capillaries via CD49e and required CXCL13 and CXCR5. During lung inflammation, marginated T2B dampened excessive neutrophil vascular inflammation via the specialized proresolving molecule lipoxin A4 (LXA4). Exogenous CXCL13 dampened excessive neutrophilic inflammation by increasing marginated B cells and LXA4 recapitulated neutrophil regulation in B-cell deficient mice during inflammation and fungal pneumonia. Thus, the lung microvasculature is enriched in multiple IgM+ B cell subsets with marginating capillary T2B that dampen neutrophil responses.
2021-07-19 | GSE156311 | GEO
Project description:Neutrophil transcriptome in community acquired pneumonia and age matched controls
| PRJNA1087440 | ENA
Project description:Neutrophils are critical in the host defense against Staphylococcus aureus, a major human pathogen. However, even in the setting of a robust neutrophil response, S. aureus can cause persistent infection. Here we demonstrate that S. aureus impairs neutrophil function by triggering the production of the anti-inflammatory metabolite, itaconate. The enzyme that synthesizes itaconate, Irg1, is selectively expressed in neutrophils during S. aureus pneumonia. Itaconate inhibits neutrophil glycolysis and oxidative burst, which impairs survival and bacterial killing. In a murine pneumonia model, neutrophil Irg1 expression protects critical lung cell populations from oxidative stress but compromises bacterial clearance. S. aureus is thus able to evade innate immune clearance by targeting neutrophil metabolism and inducing the production of the antiinflammatory metabolite itaconate.
2023-01-01 | GSE215195 | GEO
Project description:Circulating neutrophil transcriptomics in HBV-ACLF patients.
| PRJNA692986 | ENA
Project description:Rationale: Patients in the intensive care unit (ICU) are frequently exposed to unnecessary antibiotics. Markers of the host response to infection may aid pneumonia diagnosis and avoid antibiotic-induced complications. Objective: To assess the host response to suspected bacterial pneumonia through assessment of alveolar neutrophilia and transcriptomic profiling of alveolar macrophages. Methods: We determined the test characteristics of BAL neutrophilia for the diagnosis of bacterial pneumonia in 3 cohorts of mechanically ventilated patients. In one cohort, we also isolated alveolar macrophages from BAL fluid and used the transcriptome to identify signatures of bacterial pneumonia. Finally, we developed a humanized mouse model of Pseudomonas aeruginosa pneumonia to determine if pathogen-specific signatures can be identified in human alveolar macrophages. Measurements and Main Results: BAL neutrophilia was highly sensitive for bacterial pneumonia in both the retrospective (N = 851) and validation cohorts (N = 76 and N = 79) with a negative predictive value of over 90% when BAL neutrophil percentage was less than 50%. A transcriptional signature of bacterial pneumonia was present in both resident and recruited macrophages. Gene signatures from both cell types identified patients with bacterial pneumonia with test characteristics similar to BAL neutrophilia. Conclusions: A BAL neutrophil percentage of less than 50% is highly sensitive for bacterial pneumonia. Informative transcriptomic signatures can be generated from BAL fluid obtained during routine clinical care in the ICU. The identification of novel host response biomarkers is a promising approach to aid the diagnosis and treatment of pneumonia.
2018-11-06 | GSE121871 | GEO