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Differences in Mitochondrial Function in Peripheral Blood Mononuclear Cells of Patients Admitted to an Intensive Care Unit
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A1816 - Differences in Mitochondrial Function in Peripheral Blood Mononuclear Cells of Patients Admitted to an Intensive Care Unit
Author Block: L. Torres1, E. Finkelsztein2, E. Sanchez1, S. M. Cloonan1, A. M. Choi1; 1Joan and Sanford I. Weill Department of Medicine, New York-Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States, 2Department of Internal Medicine, New York Presbyterian Brooklyn Methodist Hospital, New York, NY, United States.
Rationale: Mitochondria are highly sensitive to changes in their cellular environment. Previous studies have reported mitochondrial dysfunction and redox imbalance in leukocytes of patients with sepsis (Belikova I, Crit Care Med, 2010). In addition, cellular changes in metabolism causing a shift from oxidative phosphorylation and beta-oxidation to aerobic glycolysis have been demonstrated in sepsis models using immune cells (Cheng, Nat Immunol, 2016). We have previously demonstrated that circulating mitochondrial DNA, a possible downstream effector of cellular mitochondrial dysfunction is elevated in patients admitted to the ICU, and correlates with in-hospital mortality. In this study, we sought to identify differences in cellular metabolism of peripheral blood mononuclear cells (PBMCs) in a cohort of adult patients admitted to an intensive care unit (ICU) in our hospital. Methods: After study protocol approval by the Institutional Review Board of Weill Cornell Medicine, patients were prospectively recruited for the study upon admission to the ICU. Baseline demographics, clinical details, and outcomes were recorded. Patients admitted with septic shock were compared to a control group comprising patients admitted without sepsis or septic shock. After informed consent, whole blood was collected from each patient. PBMCs were isolated and mitochondrial functional assays carried out. Using inhibitors of the electron transport chain oxygen consumption rate (OCR), a measure of mitochondrial respiration, and extracellular acidification rate (ECAR), a measure of glycolytic activity, were determined for each patient.
Results: Compared with controls (n=8), patients with septic shock (n=6) trended toward a lower maximal OCR. Patients who did not survive to hospital discharge had higher ECAR compared with survivors of septic shock and control patients.
Conclusion: Differences in mitochondrial function are seen when comparing PBMCs of patients admitted to an intensive care unit with septic shock versus those without sepsis or septic shock. Patients with septic shock showed a greater tendency toward glycolytic metabolism and impaired mitochondrial respiration. Further studies are required to assess whether other significant features of pathologic stress exist between these groups of patients.
Author Block: L. Torres1, E. Finkelsztein2, E. Sanchez1, S. M. Cloonan1, A. M. Choi1; 1Joan and Sanford I. Weill Department of Medicine, New York-Presbyterian Hospital, Weill Cornell Medicine, New York, NY, United States, 2Department of Internal Medicine, New York Presbyterian Brooklyn Methodist Hospital, New York, NY, United States.
Rationale: Mitochondria are highly sensitive to changes in their cellular environment. Previous studies have reported mitochondrial dysfunction and redox imbalance in leukocytes of patients with sepsis (Belikova I, Crit Care Med, 2010). In addition, cellular changes in metabolism causing a shift from oxidative phosphorylation and beta-oxidation to aerobic glycolysis have been demonstrated in sepsis models using immune cells (Cheng, Nat Immunol, 2016). We have previously demonstrated that circulating mitochondrial DNA, a possible downstream effector of cellular mitochondrial dysfunction is elevated in patients admitted to the ICU, and correlates with in-hospital mortality. In this study, we sought to identify differences in cellular metabolism of peripheral blood mononuclear cells (PBMCs) in a cohort of adult patients admitted to an intensive care unit (ICU) in our hospital. Methods: After study protocol approval by the Institutional Review Board of Weill Cornell Medicine, patients were prospectively recruited for the study upon admission to the ICU. Baseline demographics, clinical details, and outcomes were recorded. Patients admitted with septic shock were compared to a control group comprising patients admitted without sepsis or septic shock. After informed consent, whole blood was collected from each patient. PBMCs were isolated and mitochondrial functional assays carried out. Using inhibitors of the electron transport chain oxygen consumption rate (OCR), a measure of mitochondrial respiration, and extracellular acidification rate (ECAR), a measure of glycolytic activity, were determined for each patient.
Results: Compared with controls (n=8), patients with septic shock (n=6) trended toward a lower maximal OCR. Patients who did not survive to hospital discharge had higher ECAR compared with survivors of septic shock and control patients.
Conclusion: Differences in mitochondrial function are seen when comparing PBMCs of patients admitted to an intensive care unit with septic shock versus those without sepsis or septic shock. Patients with septic shock showed a greater tendency toward glycolytic metabolism and impaired mitochondrial respiration. Further studies are required to assess whether other significant features of pathologic stress exist between these groups of patients.
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