Transcriptomic evidence of lung repair in paediatric ARDS survival
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ABSTRACT:
PROVIDER: PRJNA928385 | ENA |
REPOSITORIES: ENA
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Project description:Pediatric patients survive from acute respiratory distress syndrome (ARDS) better than adults. However, immunological characteristics of lung tissue and peripheral circulation in pediatric ARDS has been scared. A 10-year-old girl suffered from ARDS was treated with anti-infection, anti-inflammatory regimen and with ECMO support. Air leak was fixed by surgery. Surgically dissected lung biopsies and peripheral blood cells (PBCs) were obtained from this patient and other control subjects for single cell RNA sequencing analysis. Pathological examination was also conducted on the lung biopsy. Out data revealed transcriptional characteristics of PBCs and lung microenvironment during ARDS recovery phase, and pointed out that efficient oxygen supply, appropriate immune regulation, and adequate anti-infection treatment favor for the recovery of children from ARDS.
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Project description:Rat model of ARDS was induced by saline lavage and mechanical ventilation. miRNA from rat lungs were used for dual color DNA microarray hybridization with 3DNA 50 kit version 2. Two-condition experiment, CON vs. ARDS lung tissues. replicates: 6 control, 6 ARDS. One replicate per array.
2014-05-07 | E-GEOD-57223 | biostudies-arrayexpress
Project description:Rat model of ARDS was induced by saline lavage and mechanical ventilation. Total RNA from rat lungs were used for dual color DNA microarray hybridization with 3DNA 50 kit version 2. Two-condition experiment, CON vs. ARDS lung tissues. replicates: 5 control, 7 ARDS. One replicate per array.
2014-04-24 | E-GEOD-57011 | biostudies-arrayexpress
Project description:SARS-CoV-2 is a novel coronavirus that causes acute respiratory distress syndrome (ARDS), death and long-term sequelae. Innate immune cells are critical for host defense but are also the primary drivers of ARDS. The relationships between innate cellular responses in ARDS resulting from COVID-19 compared to other causes of ARDS, such as bacterial sepsis is unclear. Moreover, the beneficial effects of dexamethasone therapy during severe COVID-19 remain speculative, but understanding the mechanistic effects could improve evidence-based therapeutic interventions. To interrogate these relationships, we developed an scRNAseq atlas that is freely accessible (biernaskielab.ca/COVID_neutrophil). We discovered that compared to bacterial ARDS, COVID-19 was associated with distinct neutrophil polarization characterized by either interferon (IFN) or prostaglandin (PG) active states. Neutrophils from bacterial ARDS had higher expression of antibacterial molecules such as PLAC8 and CD83. Dexamethasone therapy in COVID patients rapidly altered the IFNactive state, downregulated interferon responsive genes, and activated IL1R2+ve neutrophils. Dexamethasone also induced the emergence of immature neutrophils expressing immunosuppressive molecules ARG1 and ANXA1, which were not present in healthy controls. Moreover, dexamethasone remodeled global cellular interactions by changing neutrophils from information receivers into information providers. Importantly, male patients had higher proportions of IFNactive neutrophils and a greater degree of steroid-induced immature neutrophil expansion. Indeed, the highest proportion of IFNactive neutrophils was associated with mortality. These results define neutrophil states unique to COVID-19 when contextualized to other life-threatening infections, thereby enhancing the relevance of our findings at the bedside. Furthermore, the molecular benefits of dexamethasone therapy are also defined. The identified molecular pathways can now be targeted to develop improved therapeutics.
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Project description:DNA repair and autophagy are distinct biological processes vital for cell survival. Although autophagy helpsmaintain genome stability, there is no evidence of its direct role in the repair of DNA lesions. We discoveredthat lysosomes process topoisomerase 1 cleavage complexes (TOP1cc) DNA lesions in vertebrates. Selectivedegradation of TOP1cc by autophagy directs DNA damage repair and cell survival at clinically relevantdoses of topoisomerase 1 inhibitors. TOP1cc are exported from the nucleus to lysosomes through a transientalteration of the nuclear envelope and independent of the proteasome. Mechanistically, the autophagy receptorTEX264 acts as a TOP1cc sensor at DNA replication forks, triggering TOP1cc processing by theQ8 p97 ATPase and mediating the delivery of TOP1cc to lysosomes in an MRE11-nuclease- and ATR-kinasedependentmanner. We found an evolutionarily conserved role for selective autophagy in DNA repair that enQ2ables cell survival, protects genome stability, and is clinically relevant for colorectal cancer patients.
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Project description:DNA repair and autophagy are distinct biological processes vital for cell survival. Although autophagy helps maintain genome stability, there is no evidence of its direct role in the repair of DNA lesions. We discovered that in human cells, lysosomes process Topoisomerase 1-cleavage complexes (TOP1cc) DNA lesion. Selective degradation of TOP1cc by autophagy directs DNA damage repair and cell survival at clinically relevant doses of Topoisomerase 1 inhibitors. TOP1cc are exported from the nucleus to lysosomes through transient alteration of the nuclear envelope, and independent of the proteasome. Mechanistically, the autophagy receptor TEX264 acts as a TOP1cc sensor at DNA replication forks, triggering TOP1cc processing by the p97 ATPase and mediating TOP1cc delivery to lysosomes dependent on MRE11 nuclease and ATR kinase. We found an evolutionary conserved role for selective autophagy in DNA damage repair that enables cell survival, protects genome stability, and is clinically relevant for colorectal cancer patients.
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Project description:Clinical study of critically ill patients with sepsis and sepsis-related ARDS with whole blood RNA collected within the first 24 hours of admission Goal of the study was to determine whether biologically relevant genes were identified to be differentially expressed genes in patients with sepsis alone and sepsis with ARDS Prospective observational study, case cohort design
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