title: Patients with sepsis exhibit increased mitochondrial respiratory capacity in peripheral blood immune cells.
abstract: BACKGROUND
  In sepsis, mitochondria have been associated with both initial dysfunction and subsequent upregulation (biogenesis). However, the evolvement of mitochondrial function in sepsis over time is largely unknown, and we therefore investigated mitochondrial respiration in peripheral blood immune cells (PBICs) in sepsis patients during the first week after admission to the intensive care unit (ICU).
  
  
  METHODS
  PBICs from 20 patients with severe sepsis or septic shock were analyzed with high-resolution respirometry 3 times after admission to the ICU (within 48 hours, days 3 to 4 and days 6 to 7). Mitochondrial DNA (mtDNA), cytochrome c (Cyt c), and citrate synthase (CS) were measured as indicators of cellular mitochondrial content.
  
  
  RESULTS
  In intact PBICs with endogenous substrates, a gradual increase in cellular respiration reached 173% of controls after 1 week (P = 0.001). In permeabilized cells, respiration using substrates of complex I, II, and IV were significantly increased days 1 to 2, reaching 137%, 130%, and 173% of controls, respectively. In parallel, higher levels of CS activity, mtDNA, and Cyt c content in PBICs (211%, 243%, and 331% of controls for the respective indicators were found at days 6 to 7; P < 0.0001). No differences in respiratory capacities were noted between survivors and nonsurvivors at any of the time points measured.
  
  
  CONCLUSIONS
  PBICs from patients with sepsis displayed higher mitochondrial respiratory capacities compared with controls, due to an increased mitochondrial content, as indicated by increased mitochondrial DNA, protein content, and enzyme activity. The results argue against mitochondrial respiratory dysfunction in this type of cells in sepsis.
authors.forename: Fredrik
authors.initials: F
authors.lastname: Sjövall
authors.forename: Saori
authors.initials: S
authors.lastname: Morota
authors.forename: Johan
authors.initials: J
authors.lastname: Persson
authors.forename: Magnus J
authors.initials: MJ
authors.lastname: Hansson
authors.forename: Eskil
authors.initials: E
authors.lastname: Elmér
mesh_terms: D000328:Adult; D000368:Aged; D019069:Cell Respiration / Q000502:physiology; D005260:Female; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology; D007362:Intensive Care Units; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D008928:Mitochondria / Q000276:immunology / Q000378:metabolism*; D018805:Sepsis / Q000276:immunology / Q000378:metabolism*; D055815:Young Adult