title: Compartmental apoptosis and neutrophil accumulation in severe peritonitis.
abstract: BACKGROUND
  Migration and activation of polymorphonuclear neutrophils (PMN) and apoptosis are central to inflammatory tissue damage. This study examines the relation of these processes, and their expression in the abdominal, systemic, and bronchoalveolar compartments in patients with severe peritonitis.
  
  
  METHODS
  Thirty-one consecutive patients undergoing laparotomy for severe secondary peritonitis. Eight operated patients without peritonitis and 10 long-term mechanically ventilated noninfected patients served as controls. Peritoneal fluid, blood, and bronchoalveolar lavage fluid (BALF) was obtained on d 0 (day of initial laparotomy), 2, and 3. Levels of chemokines (interleukin (IL)-8 and monocyte chemotactic protein (MCP)-1), PMN-counts, PMN activation [myeloperoxidase (MPO), elastase] and apoptosis (nucleosomes) were determined.
  
  
  RESULTS
  In peritonitis patients, levels of chemokines and markers of PMN sequestration were increased in all compartments. IL-8 levels were higher in BALF than in plasma, and did not originate from the circulation or from lysis of alveolar cells. Pulmonary nucleosome levels were higher in patients who died (P=0.020), and corresponded with PMN-count in BALF (P<0.001), levels of chemokines (IL-8, P=0.003; MCP-1, P=0.001), and PMN-activation (MPO, P<0.001; elastase P=0.007).
  
  
  CONCLUSIONS
  Severe peritonitis produces an early pulmonary expression of chemoattractants creating a gradient for PMN sequestration and activation into the lung. These parameters are associated with expression of apoptosis in the lung, which is increased in nonsurviving peritonitis patients.
authors.affiliation: Department of Surgery, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: J W Olivier
authors.initials: JW
authors.lastname: van Till
authors.forename: Suzanne Q
authors.initials: SQ
authors.lastname: van Veen
authors.forename: Veronique
authors.initials: V
authors.lastname: den Broeder
authors.forename: Paul
authors.initials: P
authors.lastname: Bresser
authors.forename: Rene
authors.initials: R
authors.lastname: Lutter
authors.forename: Theo A
authors.initials: TA
authors.lastname: Out
authors.forename: Marcus J
authors.initials: MJ
authors.lastname: Schultz
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: Gouma
authors.forename: Marja A
authors.initials: MA
authors.lastname: Boermeester
mesh_terms: D018806:APACHE; D000005:Abdomen / Q000503:physiopathology; D000368:Aged; D017209:Apoptosis / Q000502:physiology*; D001992:Bronchoalveolar Lavage Fluid; D018932:Chemokine CCL2 / Q000097:blood; D002633:Chemotaxis; D005260:Female; D006801:Humans; D016209:Interleukin-8 / Q000097:blood; D007902:Length of Stay; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000502:physiology*; D009707:Nucleosomes / Q000502:physiology; D010538:Peritonitis / Q000097:blood / Q000503:physiopathology* / Q000601:surgery*; D009195:Peroxidase / Q000097:blood; D011175:Positive-Pressure Respiration
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D016209:Interleukin-8; D009707:Nucleosomes; D009195:Peroxidase