Distinct mitochondrial respiration profiles in pediatric patients with febrile illness versus sepsis
Mitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness. Prospective study of children in an Emergency Department (ED) with febrile illness or without infection (ED controls); secondary analysis of ICU patients with sepsis or without infection (ICU controls)....
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Abstract | Mitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness.
Prospective study of children in an Emergency Department (ED) with febrile illness or without infection (ED controls); secondary analysis of ICU patients with sepsis or without infection (ICU controls). Mitochondrial oxygen consumption measured in peripheral blood mononuclear cells using respirometry, with primary outcome of spare respiratory capacity (SRC). Mitochondrial content measured as citrate synthase (CS: febrile illness and ED controls) and mitochondrial to nuclear DNA ratio (mtDNA:nDNA: all groups).
SRC was lower in febrile illness (6.7 ± 3.0 pmol/sec/10
cells) and sepsis (5.7 ± 4.7) than ED/PICU controls (8.5 ± 3.7; both p < 0.05), but not different between febrile illness and sepsis (p = 0.26). Low SRC was driven by increased basal respiration in febrile illness and decreased maximal uncoupled respiration in sepsis. Differences were no longer significant after adjustment for patient demographics. Febrile illness demonstrated lower CS activity than ED controls (p = 0.07) and lower mtDNA:nDNA than both ED/PICU controls and sepsis (both p < 0.05).
Mitochondrial SRC was reduced in both febrile illness and sepsis, but due to distinct mitochondrial profiles and impacted by demographics. Further work is needed to determine if mitochondrial profiles could differentiate febrile illness from early sepsis.
Mitochondrial dysfunction has been linked to organ failure in sepsis, but whether mitochondrial alterations are evident in febrile illness without sepsis is unknown. In our study, while mitochondrial spare respiratory capacity (SRC), an index of cellular bioenergetic reserve under stress, was reduced in children with both febrile illness and sepsis compared to children without infections, low SRC was driven by increased basal respiration in febrile illness compared with decreased maximal uncoupled respiration in sepsis. Additional research is needed to understand if distinct mitochondrial profiles could be used to differentiate febrile illness from early sepsis in children. |
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AbstractList | Mitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness.OBJECTIVEMitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness.Prospective study of children in an Emergency Department (ED) with febrile illness or without infection (ED controls); secondary analysis of ICU patients with sepsis or without infection (ICU controls). Mitochondrial oxygen consumption measured in peripheral blood mononuclear cells using respirometry, with primary outcome of spare respiratory capacity (SRC). Mitochondrial content measured as citrate synthase (CS: febrile illness and ED controls) and mitochondrial to nuclear DNA ratio (mtDNA:nDNA: all groups).METHODSProspective study of children in an Emergency Department (ED) with febrile illness or without infection (ED controls); secondary analysis of ICU patients with sepsis or without infection (ICU controls). Mitochondrial oxygen consumption measured in peripheral blood mononuclear cells using respirometry, with primary outcome of spare respiratory capacity (SRC). Mitochondrial content measured as citrate synthase (CS: febrile illness and ED controls) and mitochondrial to nuclear DNA ratio (mtDNA:nDNA: all groups).SRC was lower in febrile illness (6.7 ± 3.0 pmol/sec/106 cells) and sepsis (5.7 ± 4.7) than ED/PICU controls (8.5 ± 3.7; both p < 0.05), but not different between febrile illness and sepsis (p = 0.26). Low SRC was driven by increased basal respiration in febrile illness and decreased maximal uncoupled respiration in sepsis. Differences were no longer significant after adjustment for patient demographics. Febrile illness demonstrated lower CS activity than ED controls (p = 0.07) and lower mtDNA:nDNA than both ED/PICU controls and sepsis (both p < 0.05).RESULTSSRC was lower in febrile illness (6.7 ± 3.0 pmol/sec/106 cells) and sepsis (5.7 ± 4.7) than ED/PICU controls (8.5 ± 3.7; both p < 0.05), but not different between febrile illness and sepsis (p = 0.26). Low SRC was driven by increased basal respiration in febrile illness and decreased maximal uncoupled respiration in sepsis. Differences were no longer significant after adjustment for patient demographics. Febrile illness demonstrated lower CS activity than ED controls (p = 0.07) and lower mtDNA:nDNA than both ED/PICU controls and sepsis (both p < 0.05).Mitochondrial SRC was reduced in both febrile illness and sepsis, but due to distinct mitochondrial profiles and impacted by demographics. Further work is needed to determine if mitochondrial profiles could differentiate febrile illness from early sepsis.CONCLUSIONMitochondrial SRC was reduced in both febrile illness and sepsis, but due to distinct mitochondrial profiles and impacted by demographics. Further work is needed to determine if mitochondrial profiles could differentiate febrile illness from early sepsis.Mitochondrial dysfunction has been linked to organ failure in sepsis, but whether mitochondrial alterations are evident in febrile illness without sepsis is unknown. In our study, while mitochondrial spare respiratory capacity (SRC), an index of cellular bioenergetic reserve under stress, was reduced in children with both febrile illness and sepsis compared to children without infections, low SRC was driven by increased basal respiration in febrile illness compared with decreased maximal uncoupled respiration in sepsis. Additional research is needed to understand if distinct mitochondrial profiles could be used to differentiate febrile illness from early sepsis in children.IMPACT STATEMENTMitochondrial dysfunction has been linked to organ failure in sepsis, but whether mitochondrial alterations are evident in febrile illness without sepsis is unknown. In our study, while mitochondrial spare respiratory capacity (SRC), an index of cellular bioenergetic reserve under stress, was reduced in children with both febrile illness and sepsis compared to children without infections, low SRC was driven by increased basal respiration in febrile illness compared with decreased maximal uncoupled respiration in sepsis. Additional research is needed to understand if distinct mitochondrial profiles could be used to differentiate febrile illness from early sepsis in children. Mitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness. Prospective study of children in an Emergency Department (ED) with febrile illness or without infection (ED controls); secondary analysis of ICU patients with sepsis or without infection (ICU controls). Mitochondrial oxygen consumption measured in peripheral blood mononuclear cells using respirometry, with primary outcome of spare respiratory capacity (SRC). Mitochondrial content measured as citrate synthase (CS: febrile illness and ED controls) and mitochondrial to nuclear DNA ratio (mtDNA:nDNA: all groups). SRC was lower in febrile illness (6.7 ± 3.0 pmol/sec/10 cells) and sepsis (5.7 ± 4.7) than ED/PICU controls (8.5 ± 3.7; both p < 0.05), but not different between febrile illness and sepsis (p = 0.26). Low SRC was driven by increased basal respiration in febrile illness and decreased maximal uncoupled respiration in sepsis. Differences were no longer significant after adjustment for patient demographics. Febrile illness demonstrated lower CS activity than ED controls (p = 0.07) and lower mtDNA:nDNA than both ED/PICU controls and sepsis (both p < 0.05). Mitochondrial SRC was reduced in both febrile illness and sepsis, but due to distinct mitochondrial profiles and impacted by demographics. Further work is needed to determine if mitochondrial profiles could differentiate febrile illness from early sepsis. Mitochondrial dysfunction has been linked to organ failure in sepsis, but whether mitochondrial alterations are evident in febrile illness without sepsis is unknown. In our study, while mitochondrial spare respiratory capacity (SRC), an index of cellular bioenergetic reserve under stress, was reduced in children with both febrile illness and sepsis compared to children without infections, low SRC was driven by increased basal respiration in febrile illness compared with decreased maximal uncoupled respiration in sepsis. Additional research is needed to understand if distinct mitochondrial profiles could be used to differentiate febrile illness from early sepsis in children. Abstract Objective Mitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness. Methods Prospective study of children in an Emergency Department (ED) with febrile illness or without infection (ED controls); secondary analysis of ICU patients with sepsis or without infection (ICU controls). Mitochondrial oxygen consumption measured in peripheral blood mononuclear cells using respirometry, with primary outcome of spare respiratory capacity (SRC). Mitochondrial content measured as citrate synthase (CS: febrile illness and ED controls) and mitochondrial to nuclear DNA ratio (mtDNA:nDNA: all groups). Results SRC was lower in febrile illness (6.7 ± 3.0 pmol/sec/10 6 cells) and sepsis (5.7 ± 4.7) than ED/PICU controls (8.5 ± 3.7; both p < 0.05), but not different between febrile illness and sepsis ( p = 0.26). Low SRC was driven by increased basal respiration in febrile illness and decreased maximal uncoupled respiration in sepsis. Differences were no longer significant after adjustment for patient demographics. Febrile illness demonstrated lower CS activity than ED controls ( p = 0.07) and lower mtDNA:nDNA than both ED/PICU controls and sepsis (both p < 0.05). Conclusion Mitochondrial SRC was reduced in both febrile illness and sepsis, but due to distinct mitochondrial profiles and impacted by demographics. Further work is needed to determine if mitochondrial profiles could differentiate febrile illness from early sepsis. Impact statement Mitochondrial dysfunction has been linked to organ failure in sepsis, but whether mitochondrial alterations are evident in febrile illness without sepsis is unknown. In our study, while mitochondrial spare respiratory capacity (SRC), an index of cellular bioenergetic reserve under stress, was reduced in children with both febrile illness and sepsis compared to children without infections, low SRC was driven by increased basal respiration in febrile illness compared with decreased maximal uncoupled respiration in sepsis. Additional research is needed to understand if distinct mitochondrial profiles could be used to differentiate febrile illness from early sepsis in children. |
Author | Luchette, Katherine Farooqi, Sumera Weiss, Scott L Hernandez, Tyne Sartori, Laura F Tsemberis, Elena Zhang, Donglan McCann, John C Bush, Jenny Balamuth, Fran |
Author_xml | – sequence: 1 givenname: Laura F surname: Sartori fullname: Sartori, Laura F email: sartoril@chop.edu, sartoril@chop.edu organization: University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA. sartoril@chop.edu – sequence: 2 givenname: Elena surname: Tsemberis fullname: Tsemberis, Elena organization: Department of Emergency Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, USA – sequence: 3 givenname: Tyne surname: Hernandez fullname: Hernandez, Tyne organization: Department of Emergency Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, USA – sequence: 4 givenname: Katherine surname: Luchette fullname: Luchette, Katherine organization: University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA – sequence: 5 givenname: Donglan surname: Zhang fullname: Zhang, Donglan organization: Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, USA – sequence: 6 givenname: Sumera surname: Farooqi fullname: Farooqi, Sumera organization: Nemours Children's Health, Wilmington, DE, USA – sequence: 7 givenname: Jenny surname: Bush fullname: Bush, Jenny organization: Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, USA – sequence: 8 givenname: John C surname: McCann fullname: McCann, John C organization: Department of Anesthesiology and Critical Care Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, USA – sequence: 9 givenname: Fran surname: Balamuth fullname: Balamuth, Fran organization: University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA – sequence: 10 givenname: Scott L surname: Weiss fullname: Weiss, Scott L organization: Sidney Kimmel Medical College - Thomas Jefferson University, Philadelphia, PA, USA |
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Snippet | Mitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness.
Prospective study of children in an Emergency Department (ED)... Abstract Objective Mitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness. Methods Prospective study of children in... Mitochondrial dysfunction, linked to sepsis-related organ failure, is unknown in febrile illness.OBJECTIVEMitochondrial dysfunction, linked to sepsis-related... |
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Title | Distinct mitochondrial respiration profiles in pediatric patients with febrile illness versus sepsis |
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