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Interleukin 8 in the tracheobronchial aspirate of infants acts as a neutrophil chemotactic factor in the development of chronic lung disease
Author(s) -
Takasaki JIRO,
Ogawa YUNOSUKE
Publication year - 1999
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 - 10.1046/j.1442-200x.1999.01021.x
Subject(s) - medicine , chemotaxis , interleukin 8 , respiratory distress , lung , immunology , respiratory disease , interleukin , gastroenterology , inflammation , cytokine , receptor , anesthesia
Background : We have already reported that there are some periods when a high interleukin 8 (IL‐8) concentration is observed in the tracheobronchial aspirate of infants with chronic lung disease (CLD), although the changing pattern of the IL‐8 concentration varies depending on the type of CLD. Interleukin 8 is known as a neutrophil chemotactic agent. Therefore, we asked whether IL‐8 is an important neutrophil chemotactic factor in the tracheobronchial aspirate of infants who later develop CLD. Methods and Results : We measured the neutrophil chemotactic activity of the tracheobronchial aspirate in CLD infants with or without anti‐IL‐8 antibody. Preincubation with anti‐IL‐8 immunoglobulinG resulted in a significant reduction of neutrophil chemotactic activity in the tracheobronchial aspirate. In infants with CLD following respiratory distress syndrome, there was a significant relationship between the IL‐8 concentration and the neutrophil chemotactic activity of tracheobronchial aspirate without anti‐IL‐8 antibody, although no significant relationship was seen in infants with CLD following intra‐uterine infection or with other CLD. Conclusions : Interleukin 8 in the tracheobronchial aspirate seems to play a significant role in recruiting neutrophils into the airways of patients with CLD, especially CLD following respiratory distress syndrome. We believe that in this type of CLD, IL‐8 in the lung is generated as a result of hyperoxia rather than infection. In this situation, production of other neutrophil chemotactic factors or some factors that inhibit IL‐8 activity may be insignificant.