Daily Ards Research Analysis

BACKGROUND: Continuous positive airway pressure (CPAP) is an evidence-based therapy for respiratory distress syndrome (RDS), the leading cause of death for preterm infants globally. Ethiopian Neonatal Network (ENN) teams identified a quality gap in CPAP use for preterm infants with RDS. We sought to use remote education and mentorship without additional resources to improve CPAP use in this population. METHODS: Nineteen public ENN hospitals participated in this quality improvement (QI) collaborative (September 2021 to September 2022). The primary intervention was implementation of a telementoring program. Five Ethiopian nurse-physician mentor pairs each supported 4 mentee hospitals through a remote CPAP optimization training package. Quarterly ENN collaborative meetings reviewed progress and challenges. Hospitals submitted patient-level data for all neonatal unit admissions and monthly audits. Run chart rules were used to assess for nonrandom evidence of change related to CPAP use. Preterm mortality in preintervention and postintervention periods was evaluated by a χ2 test. RESULTS: The launch of the QI collaborative with remote education and mentoring coincided with an increase in the documentation of Downes score on admission (57.8% to 95.6%) and number of preterm infants (<37 weeks' gestation) receiving CPAP (129 to 138 per month). Preterm mortality decreased significantly from preintervention (28%) to postintervention periods (21.6%) (P < .0001). CONCLUSION: Ethiopian nurse-physician mentorship pairs supporting mentee hospitals in standardizing assessments of respiratory distress and optimizing the use of CPAP increased the number of preterm infants treated with CPAP. Significant reduction in preterm mortality postintervention is encouraging as CPAP use continues to scale up globally.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is a respiratory disease linked with deregulated immune responses, leading to hyperinflammation, acute respiratory distress syndrome, and pulmonary fibrosis, often with fatal outcomes. Neutrophils play a central role in COVID-19 pathogenesis, with elevated peripheral blood neutrophil counts correlating with disease severity. Despite extensive research, the molecular processes associated with neutrophil hyperactivation in COVID-19 remain elusive. METHODS: To investigate the molecular signatures underlying neutrophil-driven pathology, we conducted transcriptome analysis in neutrophils isolated from the peripheral blood of COVID-19 patients versus healthy individuals. To evaluate the specificity of identified neutrophil signatures in COVID-19, we extended our transcriptomic analysis to neutrophils from patients with idiopathic pulmonary fibrosis (IPF), a non-infectious fibrotic lung disease. Additionally, immunofluorescence staining was performed on lung biopsy specimens from IPF patients to validate transcriptomic findings at the tissue level. RESULTS: Our analysis revealed significant transcriptional changes in COVID-19 neutrophils, particularly in pathways involved in immune regulation, inflammation, and antiviral responses. Additionally, pathways associated with autophagy and chromatin remodeling were upregulated, while translation-related processes were suppressed, indicating an increased predisposition for neutrophil extracellular trap (NET) release. This neutrophil transcriptional signature in COVID-19 appears to be associated with the previously reported deregulation of the Activin/Follistatin system in the periphery. Notably, a comparative transcriptomic analysis with neutrophils isolated from IPF patients revealed the induction of substantially overlapping inflammatory processes, suggesting common deregulated responses in COVID-19 and IPF. Consistently, significant NET formation, a hallmark of COVID-19-related inflammation, was observed within lung biopsies from IPF patients. CONCLUSION: By delineating both shared and disease-specific molecular pathways, our findings validate the critical role of neutrophils in COVID-19 and IPF pathophysiology, highlighting their involvement in balancing the inflammatory response across diverse lung diseases.

BACKGROUND: Sepsis has a high morbidity and mortality rate in critically ill patients, and acute respiratory distress syndrome (ARDS) is one of its most common outcomes. However, there is still no effective biomarker to predict the risk and outcome of ARDS induced by sepsis. METHODS: In this research, the GSE32707 dataset was acquired from the Gene Expression Omnibus (GEO) database and used to identify differentially expressed genes (DEGs). The extracellular protein-related differentially expressed genes (EP-DEGs) were filtered using the Human Protein Atlas (HPA) and UniProt databases. Functional and pathway analyses of the EP-DEGs were conducted through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Additionally, hub genes were identified using STRING, Cytoscape, MCODE, and Cytohubba. The expressions of the hub genes were analyzed in both the training set (GSE32707) and the validation set (GSE66890). The diagnostic potential of lymphocyte subsets was evaluated through ROC curve assessment in the clinical cohort. RESULTS: We identified 86 EP-DEGs from DEGs. These EP-DEGs were found to be significantly enriched in leukocyte mediated immunity. We also identified 5 key extracellular protein genes GNLY, GZMK, CST7, PTPRC and CD19. CD19 expressions were increased in both training and validation sets. ROC curves showed that CD19 expression had a higher accuracy in the diagnosis of sepsis-induced ARDS. Lymphocyte subsets analysis of clinical samples revealed that CD19 CONCLUSION: In this study, we employed bioinformatics approaches to identify potential biomarkers for sepsis-induced ARDS and further validated these findings using clinical samples. Our results suggest that peripheral CD19