Published in:
Open Access
01-12-2024 | Acute Respiratory Distress-Syndrome | Research
Using a targeted metabolomics approach to explore differences in ARDS associated with COVID-19 compared to ARDS caused by H1N1 influenza and bacterial pneumonia
Authors:
Chel Hee Lee, Mohammad M. Banoei, Mariam Ansari, Matthew P. Cheng, Francois Lamontagne, Donald Griesdale, David E. Lasry, Koray Demir, Vinay Dhingra, Karen C. Tran, Terry Lee, Kevin Burns, David Sweet, John Marshall, Arthur Slutsky, Srinivas Murthy, Joel Singer, David M. Patrick, Todd C. Lee, John H. Boyd, Keith R. Walley, Robert Fowler, Greg Haljan, Donald C. Vinh, Alison Mcgeer, David Maslove, Puneet Mann, Kathryn Donohoe, Geraldine Hernandez, Genevieve Rocheleau, Uriel Trahtemberg, Anand Kumar, Ma Lou, Claudia dos Santos, Andrew Baker, James A. Russell, Brent W. Winston, for the *ARBs CORONA I. Investigators
Published in:
Critical Care
|
Issue 1/2024
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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.