title: Clara cell secretory protein in tracheobronchial aspirates and umbilical cord serum of extremely premature infants with systemic inflammation.
abstract: BACKGROUND
  A systemic fetal inflammatory response, reflected by chorioamnionitis with funisitis, is a risk factor for bronchopulmonary dysplasia. Clara cell secretory protein (CC10), a product of pulmonary Clara cells, has anti-inflammatory properties. Local down-regulation of CC10 has been associated with inflammatory lung disease. Increased serum levels of CC10 can indicate injury to alveolar-capillary integrity.
  
  
  OBJECTIVE
  We hypothesized that extremely premature infants with a systemic fetal inflammatory response would have decreased concentrations of CC10 in tracheobronchial aspirates and that CC10 concentrations in umbilical cord serum of these infants would be increased, reflecting alveolar epithelial damage.
  
  
  METHODS
  We measured CC10 concentrations in tracheobronchial aspirates of 42 ventilated extremely premature infants during their first week of life and in umbilical cord serum of 24 of them by ELISA. Standardized histological examination of the placenta, membranes and umbilical cord was used to identify infants with funisitis.
  
  
  RESULTS
  Seventeen infants with funisitis had lower CC10 concentrations in tracheobronchial aspirates on days 1 (p < 0.01) and 3 (p < 0.05) than the remaining 25. Exogenous surfactant treatment was associated with higher CC10 concentrations on day 1 (p < 0.05). Initial leukocyte count correlated inversely with CC10 in tracheobronchial aspirates on days 1-5. Umbilical cord serum concentrations of CC10 did not differ between the infants with funisitis and the controls.
  
  
  CONCLUSIONS
  Reduced anti-inflammatory CC10 concentrations in airways of extremely premature infants with a fetal inflammatory response might make their lungs susceptible for further postnatal injuries. Umbilical cord serum CC10 is not an indicator for a fetal systemic inflammatory reaction.
authors.affiliation: Department of Pediatrics, University of Würzburg, DE-97080 Wüürzburg, Germany. thomas_w@klinik.uni-wuerzburg.de
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Thomas
authors.forename: Silvia
authors.initials: S
authors.lastname: Seidenspinner
authors.forename: Natalia
authors.initials: N
authors.lastname: Kawczyńska-Leda
authors.forename: Maria
authors.initials: M
authors.lastname: Chmielnicka-Kopaczyk
authors.forename: Alexander
authors.initials: A
authors.lastname: Marx
authors.forename: Johannes
authors.initials: J
authors.lastname: Wirbelauer
authors.forename: Marta
authors.initials: M
authors.lastname: Szymankiewicz
authors.forename: Christian P
authors.initials: CP
authors.lastname: Speer
mesh_terms: D001826:Body Fluids / Q000737:chemistry*; D001980:Bronchi / Q000378:metabolism; D001997:Bronchopulmonary Dysplasia / Q000097:blood / Q000378:metabolism; D005260:Female; D005312:Fetal Blood / Q000737:chemistry* / Q000378:metabolism; D005865:Gestational Age; D006801:Humans; D052577:Infant, Extremely Low Birth Weight / Q000097:blood / Q000378:metabolism; D007231:Infant, Newborn; D007234:Infant, Premature / Q000097:blood / Q000378:metabolism; D007235:Infant, Premature, Diseases / Q000097:blood / Q000378:metabolism; D008297:Male; D009994:Osmolar Concentration; D012121:Respiration, Artificial; D044967:Serum / Q000737:chemistry / Q000378:metabolism; D013396:Suction; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000378:metabolism*; D014132:Trachea / Q000378:metabolism; D014598:Uteroglobin / Q000032:analysis* / Q000097:blood / Q000378:metabolism
chemical_list: C556389:SCGB1A1 protein, human; D014598:Uteroglobin