title: Monocyte chemoattractant protein-1 and paraoxonase-1 and 3 levels in patients with sepsis treated in an intensive care unit: a preliminary report.
abstract: BACKGROUND
  There is considerable interest in the research of molecules modulating the acute inflammatory response in patients with sepsis. Paraoxonases (PON) are antioxidant and anti-inflammatory enzymes that inhibit the production of the monocyte chemoattractant protein-1 (MCP-1). This preliminary study investigated changes in PON status and MCP-1 concentrations in critically ill patients with severe sepsis treated in an ICU and their relationship with the evolution of disease.
  
  
  METHODS
  This was a longitudinal, prospective and observational study on 15 patients with sepsis, studied at baseline and on days 1, 2, 5, 7 and 10 of their stay in the ICU. In all the patients we measured serum PON1 and PON3 concentrations, PON1 paraoxonase and lactonase activities, serum MCP-1 concentrations, and several standard biochemical and haematological parameters.
  
  
  RESULTS
  MCP-1 concentration significantly decreased with the resolution of sepsis, and this decrease was especially important during the first 5 days of hospitalisation. PON1 and PON3 tended to decrease during the first 5 days in ICU and significantly increased in days 7 and 10. Linear regression analysis showed significant and direct correlations among serum MCP-1 concentration and lactate levels at baseline. At the end of stay, PON1 paraoxonase and lactonase activities were significantly correlated with organ system function measurements.
  
  
  CONCLUSIONS
  We observed an inverse pattern between changes in MCP-1, and PON1 and PON3 levels in patients with sepsis, this was related to the resolution of their infection after receiving treatment in an ICU.
authors.affiliation: Laboratori d'Anàlisis Clíniques, Hospital Verge de la Cinta, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Tortosa, Spain.
authors.forename: Teresa
authors.initials: T
authors.lastname: Sans
authors.forename: Anna
authors.initials: A
authors.lastname: Rull
authors.forename: Jose
authors.initials: J
authors.lastname: Luna
authors.forename: Bharti
authors.initials: B
authors.lastname: Mackness
authors.forename: Michael
authors.initials: M
authors.lastname: Mackness
authors.forename: Jorge
authors.initials: J
authors.lastname: Joven
authors.forename: Marcos
authors.initials: M
authors.lastname: Ibañez
authors.forename: Rainer
authors.initials: R
authors.lastname: Pariente
authors.forename: Marta
authors.initials: M
authors.lastname: Rodriguez
authors.forename: Xavier
authors.initials: X
authors.lastname: Ortin
authors.forename: Gaspar
authors.initials: G
authors.lastname: Masdeu
authors.forename: Jordi
authors.initials: J
authors.lastname: Camps
mesh_terms: D000368:Aged; D000595:Amino Acid Sequence; D043303:Aryldialkylphosphatase / Q000097:blood*; D018932:Chemokine CCL2 / Q000097:blood*; D005260:Female; D006801:Humans; D007362:Intensive Care Units; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D018384:Oxidative Stress / Q000502:physiology; D011446:Prospective Studies; D018805:Sepsis / Q000097:blood* / Q000201:enzymology / Q000628:therapy
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human; C113656:PON3 protein, human