title: Increased production of leukocyte microparticles with enhanced expression of adhesion molecules from activated polymorphonuclear leukocytes in severely injured patients.
abstract: BACKGROUND
  Polymorphonuclear leukocyte (PMNL)-derived microparticles (MPs) have been recently reported as activators of vascular endothelium in vitro. The objectives of the present study were to evaluate the production of MPs in severely injured patients and to clarify the role of these MPs.
  
  
  METHODS
  Thirty severely injured patients (mean Injury Severity Score of 27 +/- 11) and 21 healthy volunteers participated in the study. Blood samples were obtained serially at three time points: days 0 to 1, days 2 to 5, and days 6 to 12 after the trauma event. MP production, CD11b and CD62L expression on MPs, and oxidative activity in PMNLs were measured by flow cytometry in both the presence and absence of formylmethionyl-leucyl-phenylalanine. Expressions of CD11b and CD62L were differentially evaluated according to the size of the MPs (>or= or < 1.0 microm). Soluble E-selectin and thrombomodulin levels in blood, variables representative of systemic vascular endothelial damage, were also measured.
  
  
  RESULTS
  Production of MPs with and without formylmethionyl-leucyl-phenylalanine and the oxidative activity in PMNLs (O ) were prominently increased on days 2 to 5 after trauma. CD62L expression was enhanced on MPs at all three time points, and CD11b expression was enhanced on MPs < 1.0 microm in diameter at all three time points. Soluble E2-selectin and thrombomodulin in blood did not change significantly between time points.
  
  
  CONCLUSIONS
  Activated PMNLs enhance production of PMNL-derived MPs with increased adhesion molecule expression on days 2 to 5 after severe trauma. This response per se, however, may not progress to systemic vascular endothelial damage.
authors.affiliation: Department of Traumatology, Osaka University Medical School, 2-15 Yamadaoka, Suita City, Osaka 565-0871, Japan. fujimi@hp-emerg.med.osaka-u.ac.jp
authors.forename: Satoshi
authors.initials: S
authors.lastname: Fujimi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ogura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tanaka
authors.forename: Taichin
authors.initials: T
authors.lastname: Koh
authors.forename: Hideo
authors.initials: H
authors.lastname: Hosotsubo
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Nakamori
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Kuwagata
authors.forename: Takeshi
authors.initials: T
authors.lastname: Shimazu
authors.forename: Hisashi
authors.initials: H
authors.lastname: Sugimoto
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002097:C-Reactive Protein; D039481:CD11b Antigen / Q000032:analysis / Q000276:immunology; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000276:immunology*; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007249:Inflammation; D015601:Injury Severity Score; D019041:L-Selectin / Q000032:analysis / Q000276:immunology; D007958:Leukocyte Count; D007962:Leukocytes / Q000737:chemistry / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009104:Multiple Trauma / Q000097:blood / Q000145:classification / Q000276:immunology*; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D018375:Neutrophil Activation / Q000276:immunology*; D009504:Neutrophils / Q000737:chemistry / Q000276:immunology*; D018180:Thrombomodulin / Q000097:blood; D013997:Time Factors
chemical_list: D039481:CD11b Antigen; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D018180:Thrombomodulin; D019041:L-Selectin; D009240:N-Formylmethionine Leucyl-Phenylalanine; D002097:C-Reactive Protein