title: Evaluation of the -26G>A CC16 polymorphism in acute respiratory distress syndrome.
abstract: OBJECTIVE
  Different risk factors are presumably involved in the pathogenesis of acute respiratory distress syndrome (ARDS) including genetic factors. Clara cell protein 16 (CC16) is a potential candidate gene for ARDS susceptibility because reduced levels of the anti-inflammatory CC16 have been observed in bronchoalveolar lavage fluids or serum of patients with different inflammatory lung diseases. Furthermore, CC16 potently inhibits phospholipase A2, which plays a major role in ARDS pathophysiology. A functional polymorphism (-26G>A) was previously identified and related to decreased CC16 levels, asthma, and asthma severity.
  
  
  METHODS
  Observational study.
  
  
  METHODS
  Adults with ARDS were recruited from intensive care units in two university medical centers.
  
  
  METHODS
  We evaluated the role of this genetic variant in 117 German patients with ARDS and 373 German controls.
  
  
  METHODS
  The CC16 -26G>A polymorphism was analyzed by melting-curve analysis using a pair of fluorescence resonance energy transfer probes.
  
  
  RESULTS
  CC16 genotype frequencies in ARDS patients did not differ from those seen in controls. Also, the allele frequencies were identical in patients compared with controls (0.66 and 0.34). Moreover, only one of the patients who died (n = 27) was homozygous for the -26A allele.
  
  
  CONCLUSIONS
  The CC16 -26G>A polymorphism does not affect the susceptibility to and the outcome of ARDS.
authors.affiliation: Department of Anesthesiology, Charité, Universitätsmedizin Berlin, Berlin, Germany.
authors.forename: Ilka
authors.initials: I
authors.lastname: Frerking
authors.forename: Claudia
authors.initials: C
authors.lastname: Sengler
authors.forename: Andreas
authors.initials: A
authors.lastname: Günther
authors.forename: Hans-Dieter
authors.initials: HD
authors.lastname: Walmrath
authors.forename: Paul
authors.initials: P
authors.lastname: Stevens
authors.forename: Heiko
authors.initials: H
authors.lastname: Witt
authors.forename: Olfert
authors.initials: O
authors.lastname: Landt
authors.forename: Ulrich
authors.initials: U
authors.lastname: Pison
authors.forename: Renate
authors.initials: R
authors.lastname: Nickel
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D005260:Female; D005838:Genotype; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics*; D011379:Prognosis; D012128:Respiratory Distress Syndrome / Q000175:diagnosis / Q000235:genetics*; D014598:Uteroglobin / Q000235:genetics*
chemical_list: C556389:SCGB1A1 protein, human; D014598:Uteroglobin