title: Low level of tracheal cellular fibronectin in extremely premature infants with funisitis: relationship with respiratory distress 1 month after birth.
abstract: BACKGROUND
  Funisitis reflects the fetal systemic inflammatory response in premature infants. Macrophages and neutrophils have been identified as key elements in the inflammatory process of the lungs, and secrete proteases that cause the destruction of the extracellular matrix (ECM). Fibronectin (FN) is the major constituent of the pulmonary ECM and exists in multiple isoforms arising from alternative RNA splicing. Extra domain A (EDA) is the major alternatively spliced segment, and the expression of EDA containing FN (EDA + FN) in the lungs is associated with distal pulmonary cell proliferation during alveolar formation.
  
  
  OBJECTIVE
  To study the relationship between the presence of funisitis and EDA + FN levels in the tracheal aspirate fluid (TAF) of infants of less than 28 weeks' gestation.
  
  
  METHODS
  The subjects included in this study were 26 extremely premature infants of <28 weeks' gestation at <24 hr of age, from whom the TAF was collected. These preterm infants were divided into two groups according to placental histology. The funisitis (+) group (n = 9) was compared with the funisitis (-) group (n = 17). The TAF supernatants were analyzed for IL-1β, IL-6, IL-8, neutrophil elastase, and EDA + FN using enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  There were no significant differences in gestational age or birthweight between these groups. The funisitis (+) group had a significantly higher ventilator setting (inspired O(2)  × mean airway pressure) at Day 28 than the funisitis (-) group. In the TAF, the concentrations of IL-1β were significantly higher in the funisitis (+) group than in the funisitis (-) group, as were the concentrations of neutrophil elastase. The concentrations of EDA + FN were significantly lower in the funisitis (+) group than in the funisitis (-) group.
  
  
  CONCLUSIONS
  Decreased EDA + FN in TAF might be one of the risk factors leading to respiratory distress in extremely premature infants with funisitis.
authors.affiliation: Department of Pediatrics, Akita University Graduate School of Medicine, Akita, Japan.
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Arai
authors.forename: Tomoo
authors.initials: T
authors.lastname: Ito
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Adachi
authors.forename: Ryoji
authors.initials: R
authors.lastname: Goto
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Takahashi
mesh_terms: D002821:Chorioamnionitis / Q000378:metabolism*; D005260:Female; D005353:Fibronectins / Q000378:metabolism*; D006801:Humans; D062071:Infant, Extremely Premature / Q000378:metabolism*; D007231:Infant, Newborn; D053583:Interleukin-1beta / Q000378:metabolism; D019272:Leukocyte Elastase / Q000378:metabolism; D008297:Male; D011247:Pregnancy; D012121:Respiration, Artificial; D012127:Respiratory Distress Syndrome, Newborn / Q000378:metabolism*; D014132:Trachea / Q000378:metabolism*
chemical_list: D005353:Fibronectins; D053583:Interleukin-1beta; D019272:Leukocyte Elastase
keywords: fibronectin; funisitis; macrophage; preterm infant