AI Article Synopsis
- ARDS (Acute Respiratory Distress Syndrome) is a critical condition linked mainly to infections like COVID-19, influenza, and bacterial pneumonia, and research is focused on its mechanisms and treatment options.
- The study aims to compare metabolic profiles of ARDS caused by COVID-19, H1N1 influenza, and bacterial pneumonia to understand their unique metabolic pathways.
- Results showed distinct metabolic differences based on the infection type, indicating different underlying mechanisms in ARDS associated with each infectious cause.
Article Abstract
Rationale: Acute respiratory distress syndrome (ARDS) is a life-threatening critical care syndrome commonly associated with infections such as COVID-19, influenza, and bacterial pneumonia. Ongoing research aims to improve our understanding of ARDS, including its molecular mechanisms, individualized treatment options, and potential interventions to reduce inflammation and promote lung repair.
Objective: To map and compare metabolic phenotypes of different infectious causes of ARDS to better understand the metabolic pathways involved in the underlying pathogenesis.
Methods: We analyzed metabolic phenotypes of 3 ARDS cohorts caused by COVID-19, H1N1 influenza, and bacterial pneumonia compared to non-ARDS COVID-19-infected patients and ICU-ventilated controls. Targeted metabolomics was performed on plasma samples from a total of 150 patients using quantitative LC-MS/MS and DI-MS/MS analytical platforms.
Results: Distinct metabolic phenotypes were detected between different infectious causes of ARDS. There were metabolomics differences between ARDSs associated with COVID-19 and H1N1, which include metabolic pathways involving taurine and hypotaurine, pyruvate, TCA cycle metabolites, lysine, and glycerophospholipids. ARDSs associated with bacterial pneumonia and COVID-19 differed in the metabolism of D-glutamine and D-glutamate, arginine, proline, histidine, and pyruvate. The metabolic profile of COVID-19 ARDS (C19/A) patients admitted to the ICU differed from COVID-19 pneumonia (C19/P) patients who were not admitted to the ICU in metabolisms of phenylalanine, tryptophan, lysine, and tyrosine. Metabolomics analysis revealed significant differences between C19/A, H1N1/A, and PNA/A vs ICU-ventilated controls, reflecting potentially different disease mechanisms.
Conclusion: Different metabolic phenotypes characterize ARDS associated with different viral and bacterial infections.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10900651 | PMC |
| http://dx.doi.org/10.1186/s13054-024-04843-0 | DOI Listing |
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