title: Paradoxical cytoskeleton and microparticle formation changes in monocytes and polymorphonuclear leukocytes in severe systemic inflammatory response syndrome patients.
abstract: BACKGROUND
  Circulating monocytes and polymorphonuclear leukocytes (PMNLs) are considered as central regulators controlling systemic inflammatory response after severe insults. Recently, activated monocytes and PMNLs have been reported to produce microparticles (MPs) in vitro. The objective of this study was to evaluate production of MPs and changes of cytoskeleton in monocytes from severe systemic inflammatory response syndrome (SIRS) patients, and to compare them with those in PMNLs.
  
  
  METHODS
  Twenty severe SIRS patients (SIRS criteria and serum C-reactive protein > 10 mg/dL) and 15 healthy volunteers were included. MP formation and F-actin content in monocytes and PMNLs were measured by flow cytometry in the presence or absence of lipopolysaccharide or formylmethionyl-leucyl-phenylalanine (FMLP). The membrane expression of human leukocyte antigen-DR and CD64 in monocytes and O2- production in PMNLs were also measured by flow cytometry.
  
  
  RESULTS
  In severe SIRS patients, MP formation with and without lipopolysaccharide in monocytes significantly decreased in comparison with those in normal controls (p < 0.05), whereas those with and without FMLP in PMNLs increased (p < 0.05). F-actin content with and without FMLP in monocytes also significantly decreased in patients (p < 0.05), whereas those in PMNLs increased as compared with normal controls (p < 0.05). The expression of human leukocyte antigen-DR in monocytes significantly decreased in patients (p < 0.05), which indicated monocyte modulation. The O2- production in PMNLs increased in patients (p < 0.05), which showed PMNL activation.
  
  
  CONCLUSIONS
  The changes of MP formation and cytoskeleton in circulating monocytes and PMNLs were paradoxically different in severe SIRS patients.
authors.affiliation: Department of Traumatology, Suita-shi, Osaka University Medical School, Japan. itakura@hp-emerg.med.osaka-u.ac.jp
authors.forename: Yuka
authors.initials: Y
authors.lastname: Itakura Sumi
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: Kieko
authors.initials: K
authors.lastname: Fujita
authors.forename: Satoshi
authors.initials: S
authors.lastname: Fujimi
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Nakamori
authors.forename: Takeshi
authors.initials: T
authors.lastname: Shimazu
authors.forename: Hisashi
authors.initials: H
authors.lastname: Sugimoto
mesh_terms: D008841:Actin Cytoskeleton / Q000378:metabolism / Q000473:pathology; D000199:Actins / Q000032:analysis* / Q000378:metabolism / Q000648:ultrastructure; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D003599:Cytoskeleton / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005434:Flow Cytometry; D006684:HLA-DR Antigens / Q000032:analysis / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007958:Leukocyte Count; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000737:chemistry / Q000378:metabolism / Q000473:pathology*; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000008:administration & dosage; D009504:Neutrophils / Q000737:chemistry / Q000378:metabolism / Q000473:pathology*; D010084:Oxidation-Reduction; D017452:Receptors, IgG / Q000032:analysis / Q000378:metabolism; D012720:Severity of Illness Index; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000209:etiology / Q000276:immunology / Q000378:metabolism
chemical_list: D000199:Actins; D006684:HLA-DR Antigens; D008070:Lipopolysaccharides; D017452:Receptors, IgG; D009240:N-Formylmethionine Leucyl-Phenylalanine; D002097:C-Reactive Protein