title: Natural inhibitors of neutrophil function in acute respiratory distress syndrome.
abstract: OBJECTIVE
  Neutrophils play a key role in the physiopathogenesis of acute lung injury in general and acute respiratory distress syndrome (ARDS) in particular. To identify the anti-inflammatory mediators with a protective effect on lung tissue damage in ARDS, we correlated the concentration of the Clara cell 16-kD protein (CC16; an inhibitor of neutrophil chemotaxis), angiogenin (an inhibitor of degranulation), and the total radical oxygen neutralizing activity with the amount of elastase (a marker of neutrophil activation) and with the Pao2/Fio2 ratio, which is inversely related to lung injury.
  
  
  METHODS
  University hospital.
  
  
  METHODS
  Patients with ARDS (n = 12) and patients at risk for developing ARDS (n = 14).
  
  
  METHODS
  Patients underwent bronchoalveolar lavage 12 hrs after diagnosis of ARDS or at-risk status.
  
  
  RESULTS
  The amount of CC16 and radical oxygen neutralizing activity was not significantly different in patients with or at risk for ARDS. In contrast, the amount (mean +/- sem) of angiogenin in the bronchoalveolar lavage of ARDS patients (45 +/- 14 ng/mL, n = 12) was increased 11-fold (p <.05) compared with patients at risk for ARDS (4 +/- 1 ng/mL, n = 14). In patients with ARDS, the amount of protein and angiogenin in bronchoalveolar lavage increased with decreasing concentration of CC16 (p <.05). In addition, CC16 correlated with the Pao2/Fio2 ratio (p <.05) and inversely with the amount of elastase (p <.05) and thus may be regarded as a reliable protective agent for lung injury.
  
  
  CONCLUSIONS
  A high concentration of CC16, a natural inhibitor of neutrophil function, decreases neutrophil-mediated lung damage of patients with ARDS. Strategies to increase natural anti-inflammatory agents, and thus influence the disruption of the balance between natural inflammatory and anti-inflammatory or protective factors, could be useful to modulate the tissue destruction and the course of ARDS.
authors.affiliation: Department of Biochemistry, Laboratory of Cellular Biochemistry, University of Antwerp, Wilrijk-Antwerpen, Belgium.
authors.forename: L
authors.initials: L
authors.lastname: Geerts
authors.forename: P G
authors.initials: PG
authors.lastname: Jorens
authors.forename: J
authors.initials: J
authors.lastname: Willems
authors.forename: M
authors.initials: M
authors.lastname: De Ley
authors.forename: H
authors.initials: H
authors.lastname: Slegers
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D018893:Bronchoalveolar Lavage; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology*; D010450:Endopeptidases / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000378:metabolism*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000502:physiology*; D010196:Pancreatic Elastase / Q000378:metabolism; D011379:Prognosis; D011446:Prospective Studies; D011506:Proteins / Q000032:analysis*; D012128:Respiratory Distress Syndrome / Q000175:diagnosis* / Q000453:epidemiology; D012259:Ribonuclease, Pancreatic / Q000032:analysis*; D012307:Risk Factors; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D014598:Uteroglobin
chemical_list: D004791:Enzyme Inhibitors; D018836:Inflammation Mediators; D011506:Proteins; C556389:SCGB1A1 protein, human; D014598:Uteroglobin; C046366:angiogenin; D012259:Ribonuclease, Pancreatic; D010450:Endopeptidases; D010196:Pancreatic Elastase