title: Biological response modifiers in photochemically pathogen-reduced versus untreated apheresis platelet concentrates.
abstract: BACKGROUND
  Lipids and other biologically active substances accumulate in platelet concentrates (PCs) during storage. Some of these substances have been suggested to modulate immune responses and to play a pathogenic role in the development of transfusion-related acute lung injury. This study compared the content and impact of some biological response modifiers in PCs treated with pathogen reduction (PR) technology and nontreated PCs.
  
  
  METHODS
  Apheresis PCs (n = 12) were split in two: one split was subjected to PR treatment (INTERCEPT, Cerus Corp.) and the other split was left untreated. Basic characterization and content of vascular endothelial growth factor (VEGF) and sCD154 were measured. Lipopolysaccharide (LPS)-induced secretion of interleukin-10 (IL-10) and tumor necrosis factor-α (TNF-α) was measured after incubation of heparinized whole blood with platelet (PLT) supernatants. The supernatants' neutrophil (PMN)-priming capacity, and thereby activation of the NADPH oxidase, was measured as the rate of superoxide anion production after formyl-Met-Leu-Phe activation. Lipids were extracted from the supernatants on Day 6 and tested for PMN-priming activity.
  
  
  RESULTS
  Supernatants from PR-treated PCs demonstrated significantly higher mean PLT volume (MPV) and O(2) , lower pH, CO(2) , and HCO(3-) , and significantly less LPS-induced TNF-α secretion compared to untreated PCs. No differences in swirling, PLT count, potassium levels, glucose consumption, lactate production, IL-10, VEGF, sCD154, or PMN-priming activity were found between the groups over time.
  
  
  CONCLUSIONS
  INTERCEPT PR treatment caused no substantial differences in PCs, except for minor changes in MPV and metabolic variables. Further studies are needed to explain the differences in the LPS-induced TNF-α secretion.
authors.affiliation: Department of Immunology and Transfusion Medicine, Oslo University Hospital, Ullevaal, Oslo, Norway. annette.vetlesen@medisin.uio.no
authors.forename: Annette
authors.initials: A
authors.lastname: Vetlesen
authors.forename: Mohammad Reza
authors.initials: MR
authors.lastname: Mirlashari
authors.forename: Ciğdem Akalın
authors.initials: CA
authors.lastname: Akkök
authors.forename: Marguerite R
authors.initials: MR
authors.lastname: Kelher
authors.forename: Samina Y
authors.initials: SY
authors.lastname: Khan
authors.forename: Christopher C
authors.initials: CC
authors.lastname: Silliman
authors.forename: Jens
authors.initials: J
authors.lastname: Kjeldsen-Kragh
mesh_terms: D001781:Blood Component Removal; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D016753:Interleukin-10 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D010777:Photochemistry; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D016753:Interleukin-10