Background: It is currently unknown if interleukin (IL)-16 exists in the lungs of ventilated infants, and because the predominant cells in the airways of infants with CLD are CD4+ macrophages, we hypothesized that IL-16 plays a role as a pro-inflammatory mediator in lung inflammation.
Aims: To examine if IL-16, a chemoattractant for CD4+ cells, is detectable in airway secretions of ventilated newborns. Its presence may be associated with lung inflammatory responses.
Study design: Cohort cross-sectional study.
Subjects: Thirty-four mechanically ventilated newborn infants.
Main outcome measures: Tracheal fluid (TF) specimens collected during the first month of life were examined for cell differentials determined from cytospin slides and supernatant was analyzed by ELISA for IL-16.
Results: Eighty-three cross-sectional tracheal fluid (TF) specimens were analyzed. Eleven of the 27 preterm but none of the 7 term infants developed chronic lung disease (CLD). IL-16, ranging from 203 to 42,073 pg/ml, was detected in 16 of the 46 specimens obtained from CLD infants, 1 of the 30 specimens from 16 non-CLD preterm and 2 of the 7 specimens from 7 term infants (p<0.001). Leukocyte counts (median 16.6 vs. 2.0 x 10(-9)/l, p<0.0001) and percentage neutrophils (median 93% vs. 73%, p<0.001) were higher in IL-16 positive specimens.
Conclusion: IL-16 is detectable within the airway secretions of ventilated newborn infants and its presence is associated with a neutrophilic infiltration. Further studies are required to investigate its role in chronic inflammation in CLD.