Daily Ards Research Analysis

PURPOSE: Blunt chest trauma is common in polytraumatised patients and often leads to respiratory distress. Moreover, the systemic inflammation resulting from the trauma itself, along with subsequent surgical interventions, further contributes to pulmonary dysfunction. Therefore, modulating post-traumatic immune responses may offer potential benefits. MicroRNAs may influence the activation and progression of regenerative responses following polytrauma and could serve as potential modulators. This study investigates the expression of a selection of miRNAs with known involvement in pulmonary pathologies relevant for the post-trauma setting, in a porcine polytrauma model comparing two surgical treatment groups and one treatment group that additionally received a drug-based treatment based on combined inhibition of complement component C5 and the Toll-like co-receptor CD14. METHODS: The porcine polytrauma model consisted of blunt chest trauma, bilateral femur fractures, liver laceration, and haemorrhagic shock. Four groups were defined: sham, early total care (ETC: n = 8), damage control orthopaedics (DCO: n = 8), ETC with C5/CD14 inhibition (n = 4). Animals were monitored and guideline-treated in an ICU setting for 72 h. After sacrifice, lung samples were taken from the left lobe. MiRNAs were analysed by qPCR. Furthermore, Periodic Acid Schiff staining and in situ hybridisation were performed. RESULTS: MiRNAs associated with lung function, inflammation, and fibrosis were analysed. Compared to ETC, DCO resulted in less inflammatory and fibrotic miRNA expression, consistent with histological findings showing more preserved alveoli, less septal thickening, and fewer inflammatory cell infiltrations. The addition of C5/CD14 inhibitors to ETC further reduced the expression of inflammatory and fibrotic microRNAs compared to both DCO and ETC and revealed a significant reduction in histopathological changes in the lung tissue. CONCLUSION: This study indicates that combined inhibition of C5 and CD14 effectively reduces posttraumatic histopathological changes in lung tissue associated with less inflammatory and fibrotic miRNA expression, compared to both the DCO and ETC groups.

BACKGROUND: Sepsis frequently results in complications such as acute respiratory distress syndrome (ARDS) and cardiomyopathy. This study aims to identify common diagnostic markers and elucidate the underlying mechanisms of these sepsis-induced complications. METHODS: We obtained datasets related to ARDS and sepsis-induced cardiomyopathy (SIC) from the GEO database and applied weighted gene co-expression network analysis (WGCNA) to identify differentially expressed genes (DEGs), which were integrated with key module genes. Feature genes were selected using support vector machine-recursive feature elimination (SVM-RFE) and random forest (RF) algorithms. An artificial neural network (ANN) model was constructed and its diagnostic performance was evaluated using receiver operating characteristic (ROC) curves. Machine learning algorithms effectively identified key hub genes associated with sepsis-induced ARDS and cardiomyopathy, with their robustness validated through ROC analysis. A cellular model of sepsis-induced lung injury was employed to examine hub gene expression. Additionally, we investigated inflammation and immune responses by characterizing immune landscapes using CIBERSORT and performing correlation analyses among feature genes, immune infiltration, and clinical characteristics. Finally, potential small-molecule compounds were identified from the PubChem database. RESULTS: Five key genes-LCN2, AIF1L, STAT3, SOCS3 and SDHD-were identified. SOCS3 showed strong diagnostic potential with gene set enrichment analysis (GSEA) highlighting its role in biological processes and immune responses. SOCS3 expression correlated strongly with immune cells. Dexamethasone, resveratrol and curcumin were identified as potential SOCS3-targeting drugs. CONCLUSION: Five genes were identified as diagnostic biomarkers for sepsis-induced ARDS and cardiomyopathy, with SOCS3 serving as a key hub gene and potential therapeutic target.

BACKGROUND/OBJECTIVES: Treatment of severe traumatic brain injury (TBI) remains a major challenge in neurocritical care. The functional state of the brain largely depends on the applied ventilation strategy. Many patients develop acute respiratory distress syndrome (ARDS), for which lung-protective ventilation is recommended. However, its effect on outcomes in severe TBI remains unclear. This study aimed to assess whether a lung-protective ventilation strategy improves short-term outcomes in patients with severe TBI complicated by ARDS. METHODS: This multicenter retrospective study included patients with severe TBI and ARDS treated in three Ukrainian tertiary hospitals. Lung-protective ventilation was defined as the use of a low tidal volume and moderate positive end-expiratory pressure (PEEP). The primary endpoint was 28-day mortality; secondary endpoints included the Glasgow Coma Scale (GCS) score and intracranial pressure (ICP) on day 28. Univariate and multivariate logistic regression analyses identified factors associated with mortality. RESULTS: Mortality did not depend on arterial PaO CONCLUSIONS: Lung-protective ventilation is safe and effective in severe TBI with ARDS, significantly improving short-term survival without compromising cerebral outcomes.