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Interleukin 8 and granulocyte elastase α 1 proteinase inhibitor complex in the tracheobronchial aspirate of infants with chronic lung disease following respiratory distress syndrome
Author(s) -
TAKASAKI JIRO,
OGAWA YUNOSUKE
Publication year - 1996
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.1996.tb03522.x
Subject(s) - medicine , elastase , respiratory distress , lung , neutrophil elastase , interleukin 1β , proteinase inhibitor , granulocyte , respiratory disease , gastroenterology , lung disease , interleukin , airway , respiratory system , pathology , immunology , enzyme , anesthesia , inflammation , biochemistry , cytokine , chemistry
In order to elucidate the role of interleukin 8 (IL‐8) on the development of chronic lung disease (CLD) in neonates following an episode of respiratory distress syndrome (RDS), serial and simultaneous measurements of the concentration of IL‐8 and granulocyte elastase α 1 proteinase inhibitor complex (E‐α 1 PI) in the tracheobronchial aspirate of very low birthweight infants with RDS were conducted. The concentration of IL‐8 and E‐α 1 PI in infants with CLD was low in the first 48 h of life, but dramatically increased after 48 h. The concentration of IL‐8 between 48 h of life and day 5 was significantly correlated to the fraction of inspired oxygen concentration ( F 1 o 2 ) within 48 h of age, but not to the mean airway pressure. Interleukin 8 seemed to stimulate neutrophils to release granulocyte elastase which, in turn, caused lung tissue injury, resulting in the development of CLD. It is suggested that high F 1 o 2 is an important factor causing IL‐8 production in the lung.